HIV transmission and cure through nutrition

[Comte de Saint-Germain]

Is there any basis for this:



I would think not, but the guy wrote the book on HIV and he's a Nobel laureate..

[Azathoth]

I wonder if that guy is a catholic. Advocating genital hygeine and nutrition rather than condom use stinks of papist claptrappery to me

[cherries]

ridiculous,does he propose to prescribe fruits to combat HIV infections to africans?what about HIV infected westerners,i guess if they just would have eaten a balanced diet they would have been able to fight of the disease.
what about condoms or this..

Fight HIV with HIV: 'safe' virus proposed as vaccine

A company is planning to inject people with an HIV vaccine made of the deadly virus itself, albeit a deactivated version.

Vaccines against many viruses, including flu, are made from deactivated versions of those viruses, but such an approach was previously dismissed as too risky in the case of HIV.

Now Virxsys of Gaithersburg, Maryland, is resurrecting the controversial approach, thanks to successful tests of a similar vaccine against SIV – also known as simian HIV – in monkeys.

"We said 'let's use HIV against itself', and that's what we're doing," says Gary McGarrity, Virxsys's vice president of scientific and clinical affairs....

http://www.newscientist.com/article/dn1 ... nline-news

[Comte de Saint-Germain]

To be honest, I was more looking for an article about him being incorrect. I mean, the guy, Luc Antoine Montagnier, is a Nobel Laureate in Medicine on this precise field. He's a virologist and one of the people that discovered HIV.

[cherries]

right,i checked it and hes not saying that having a healthy immune system is the thing to replace everything else,like medical research,use of condoms etc. but rather just a part of it.

Dr. Robert C. Gallo and Dr. Luc Montagnier
Dr. Robert C. Gallo and Dr. Luc Montagnier

25 Years After HIV Discovery: A Global Call to Action

Today we call on international organizations and governments to immediately implement six objectives to end the HIV/AIDS pandemic. We made this announcement and were joined by Jeff Crowley, Director, White House Office of National AIDS Policy.

Globally, many are acting as though HIV and AIDS are no longer the threat they were 25 years ago when the HIV virus was first discovered. However, in fact they remain an unparalleled global health threat, and despite progress in treatment, they could worsen unless determined action is taken. We believe these recommendations are key to reducing and ultimately minimizing the devastation of HIV and AIDS.

Our Global Call to Action is as follows:

1. Invest in medical infrastructure and educational outreach programs in U.S. communities most affected by the HIV/AIDS epidemic

2. Promote global development of HIV/AIDS treatment and control programs along with regional research institutions in developing countries

3. Cultivate and inspire young scientists in the field of human virology

4. Enhance HIV/AIDS education and prevention, especially in countries with high infection rates

5. Support cutting-edge vaccine research and the development of new effective therapies

6. Continue the focus on preventing mother-to-child HIV transmission

Here we are, 25 years after discovering the cause of AIDS and we still have a major, public health HIV/AIDS crisis. Never in the history of mankind have we so quickly identified the cause of an epidemic, developed a test for it and begun to develop drug therapy, changing a once-deadly virus to a lifelong condition with proper medical intervention. It is important for governments and organizations from around the world to come together and combat this collective HIV/AIDS emergency....

http://www.huffingtonpost.com/dr-robert ... 00085.html

[Agrippina]

Sounds like the sort of thing our erstwhile (and late) Minister of Health and her president were saying years ago. She advocated African potato, garlic and beetroot.
Here's some data.

According to media reports infections are dropping since the policy towards anti-retrovirals has changed and people are able to get free treatment from local clinics. We still have a huge number of deaths and burials every week and our coffin makers and funeral parlours are making millions, and of course the AIDS orphans are still a problem

[Xamonas Chegwé]

Sounds like the sort of thing our erstwhile (and late) Minister of Health and her president were saying years ago. She advocated African potato, garlic and beetroot.
Here's some data.

According to media reports infections are dropping since the policy towards anti-retrovirals has changed and people are able to get free treatment from local clinics. We still have a huge number of deaths and burials every week and our coffin makers and funeral parlours are making millions, and of course the AIDS orphans are still a problem

When you say 'our', which part of the world are you referring to? Or is this a general 'our'?

Sorry, but your Location field is not filled in.

[Rob]

This is anti-science and rhetorical nonsense of the highest degree. First off let's talk about the basis of this video. The House of Numbers interviewed a number of scientists, many of whom have responded saying they were interviewed under false pretenses(similar to Expelled), as well as Christine Maggiore. For those who do not know who she is, or why she is important enough to bring up take a quick look at this. Oddly enough, considering she died prior to the release of the film, it never mentioned that she died. Putting aside the sad story of how a woman willingly led her daughter to her grave, let's consider the parties who were interviewed during for the film. Dr. Daniel Kuritzkes among many others held a open panel of sorts, stating their position on being interviewed under false pretenses and the overall quality of information presented in the film. Additionally there is an article by The Lancet which lays it on the table quite nicely. (doi:10.1016/S1473-3099(09)70316-0 for those who have access to it through a school library). I wish I could get my hands on that article from home, I would have to go to my school to get it.

Anyhow, The House of Numbers is a nice little piece of pseudoscience which ought to be placed next to Expelled and The case against Gravity: A scientific inquiry.

[Comte de Saint-Germain]

Perhaps, but the man makes some interesting comments. Are these factually incorrect? Per example, a body with a good immune system, can it fight off HIV?

By the way, with these allegations I feel I should point out that I have no vested interest in this. I posted it here because I was genuinely curious, but I biochemistry and virology aren't things I'm sufficiently qualified in to confidently research this myself. It's just that the man has some impressive credentials that I feel anxious about dismissing his claims without evidence to the contrary.

[Rob]

Trigger Warning!!!1! :

AIDS. 2009 Jan 14;23(2):161-75.

The 'immunologic advantage' of HIV-exposed seronegative individuals.

Miyazawa M, Lopalco L, Mazzotta F, Lo Caputo S, Veas F, Clerici M; ESN Study Group.

AIDS Res Hum Retroviruses. 2008 Nov;24(11):1415-27.

Impaired viral entry cannot explain reduced CD4+ T cell susceptibility to HIV type 1 in certain highly exposed individuals.

Speelmon EC, Livingston-Rosanoff D, Desbien AL, Lee J, Wick WD, Hladik F, McElrath MJ.
Medical Scientist Training Program, University of Washington, Seattle, Washington 98105, USA.

Rare individuals report repeated unprotected HIV-1 sexual exposures, yet remain seronegative for years. We investigated the possibility that reduced in vitro CD4(+) T cell susceptibility to HIV-1 infection protects such highly exposed seronegative (ES) individuals. Susceptibility to three R5-tropic HIV-1 isolates, regardless of inoculating dose, was remarkably similar between 81 ES and 33 low-risk controls. In 94% (99/105) of donors, we observed a 1.36 log-unit range in HIV-1(JR-CSF) production, with similar results for HIV-1(1192). The median frequency of intracellular Gag(+) T cells after single-round infection was similar in ES (5.2%) and controls (7.2%), p = 0.456. However, in repeated testing, CD4(+) T cells from two controls (6.1%) and four ES (4.9%) exhibited a 10- to 2500-fold reduction in HIV-1 production and required 5- to 12-fold greater HIV-1(1192) and HIV-1(JR-CSF) inocula to establish infection (TCID(50)). Reduced viral entry cannot explain the low producer phenotype; no differences in CCR5 receptor density or beta-chemokine production were observed. In conclusion, we have identified a remarkably narrow range of HIV-1 susceptibility in seronegative donors regardless of risk activity, which can be applied as a benchmark to assess vaccine-induced antiviral effector activities. However, CD4(+) T cells from a subset of individuals demonstrated reduced HIV-1 susceptibility unexplained by impaired entry, lending support to the possibility that cellular restriction of HIV-1 may account for continued seronegativity in some of those having repeated sexual exposure. Identifying the host-virus interactions responsible for diminished in vitro susceptibility may contribute to the development of novel therapeutic strategies.

Curr HIV Res. 2008 Nov;6(6):531-8.

Increased levels of human beta-defensins mRNA in sexually HIV-1 exposed but uninfected individuals.

Zapata W, Rodriguez B, Weber J, Estrada H, Quiñones-Mateu ME, Zimermman PA, Lederman MM, Rugeles MT.

Group of Immunovirology, School of Medicine, University of Antioquia, Medellín, Colombia.

Protection against HIV-1 infection in exposed seronegative (ESN) individuals likely involves natural resistance mechanisms that have not been fully elucidated. Human beta defensins (HBD) are antimicrobial peptides found primarily in mucosae, the main ports of HIV entry. HBD-2 and 3 mRNA are induced by HIV-1 in human oral epithelial cells and exhibit strong anti-HIV-1 activity; in addition, polymorphisms in the DEFB1 gene, which encodes HBD-1, have been associated with resistance/susceptibility to different infections, including HIV-1. Here, we have assessed the association of HBD expression with the ESN phenotype. Peripheral blood and vaginal/endocervical and oral mucosal samples were taken from 47 ESN, 44 seropositive (SP) and 39 healthy controls (HC). HBD-1, 2 and 3 mRNA copy numbers were quantified by real time RT-PCR and A692G/G1654A/A1836G polymorphisms in the DEFB1 gene were detected by restriction fragment length polymorphisms and confirmed by nucleotide sequencing. ESN expressed significantly greater mRNA copy numbers of HBD-2 and 3 in oral mucosa than HC; p=0.0002 and p=0.007, respectively. mRNA copy numbers of HBD-1, 2 and 3 in vaginal/endocervical mucosa from ESN and HC were similar. Homozygosity for the A692G polymorphism was significantly more frequent in ESN (0.39) than in SP (0.05) (p=0.0002). In summary, ESN exhibited enhanced mucosal expression of the innate defense genes HBD-2 and 3; however, additional studies are required to verify these results and the potential association of the A692G polymorphism to the relative resistance of ESN to HIV-1 infection.

AIDS. 2008 Mar 30;22(6):727-35.

HIV-neutralizing immunoglobulin A and HIV-specific proliferation are independently associated with reduced HIV acquisition in Kenyan sex workers.

Hirbod T, Kaul R, Reichard C, Kimani J, Ngugi E, Bwayo JJ, Nagelkerke N, Hasselrot K, Li B, Moses S; Kibera HIV Study Group, MacDonald KS, Broliden K.
Collaborators (16)

Infectious Diseases Unit, Department of Medicine, Solna, Center for Molecular Medicine, Karolinska Institutet, Karolinska University Hospital, Solna, Sweden.

OBJECTIVES: HIV-neutralizing immunoglobulin A (IgA) and HIV-specific cellular immunity have been described in highly exposed, persistently seronegative (HEPS) individuals, but well controlled studies have not been performed. We performed a prospective, nested case-control study to examine the association of genital IgA and systemic cellular immune responses with subsequent HIV acquisition in high-risk Kenyan female sex workers (FSWs). DESIGN AND METHODS: A randomized trial of monthly antibiotic prophylaxis to prevent sexually transmitted disease/HIV infection was performed from 1998 to 2002 in HIV-uninfected Kenyan FSWs. After the completion of trial, FSWs who had acquired HIV (cases) were matched 1: 4 with persistently uninfected controls based on study arm, duration of HIV-seronegative follow-up, and time of cohort enrolment. Blinded investigators assayed the ability at enrolment of genital IgA to neutralize primary HIV isolates as well as systemic HIV-specific cellular IFNgamma-modified enzyme-linked immunospot and proliferative responses. RESULTS: The study cohort comprised 113 FSWs: 24 cases who acquired HIV and 89 matched controls. Genital HIV-neutralizing IgA was associated with reduced HIV acquisition (P = 0.003), as was HIV-specific proliferation (P = 0.002), and these associations were additive. HIV-specific IFNgamma production did not differ between case and control groups. In multivariable analysis, HIV-neutralizing IgA and HIV-specific proliferation each remained independently associated with lack of HIV acquisition. Genital herpes (HSV2) was associated with increased HIV risk and with reduced detection of HIV-neutralizing IgA. CONCLUSION: Genital HIV-neutralizing IgA and systemic HIV-specific proliferative responses, assayed by blinded investigators, were prospectively associated with HIV nonacquisition. The induction of these immune responses may be an important goal for HIV vaccines.

AIDS. 2008 May 31;22(9):1029-38.

Associations of human leukocyte antigen DRB with resistance or susceptibility to HIV-1 infection in the Pumwani Sex Worker Cohort.

Lacap PA, Huntington JD, Luo M, Nagelkerke NJ, Bielawny T, Kimani J, Wachihi C, Ngugi EN, Plummer FA.

National Microbiology Laboratory, Winnipeg, Canada.

OBJECTIVE: A group of commercial sex workers in the Pumwani Sex Worker Cohort, established in 1985 in Nairobi, Kenya, remain HIV-1 uninfected despite heavy exposure to HIV-1 through active sex work. Previous studies showed that this resistance is associated with a strong CD4+ T-cell response, which suggested that human leukocyte antigen class II antigens are important in resistance/susceptibility to HIV-1 infection. DRB1 is the most polymorphic locus among class II genes and forms haplotypes with DRB3, DRB4 and DRB5. The aim of this study is to investigate the role of DRB alleles/haplotypes on resistance/susceptibility to HIV-1 infection. DESIGN: In total, 1090 women enrolled in the Pumwani cohort were genotyped for DRB1, DRB3, DRB4 and DRB5 using a high-resolution sequence-based method. Allele/haplotype frequencies were compared between HIV-positive women and women who have remained HIV negative for more than 3 years despite frequent exposure. METHODS: Human leukocyte antigen DRB genes were amplified, sequenced and genotyped using a two-step sequence-based method. Allele/haplotype frequencies were determined using PyPop32-0.6.0. Statistical analysis was conducted using SPSS 11.0 for Windows. RESULTS: Three DRB1 alleles were associated with resistance: DRB1*010101 (P = 0.016; odd ratio (OR): 2.55; 95% confidence interval (CI): 1.16-5.61), DRB1*010201 (P = 0.019; OR: 1.86; 95% CI: 1.10-3.15), and DRB1*1102 (P = 0.025; OR: 1.72; 95% CI: 1.07-2.78). DRB1*030201 (P = 0.038; OR: 0.48; 95% CI: 0.23-0.98), DRB1*070101 (P = 0.035; OR: 0.54; 95% CI: 0.30-0.97), DRB1*1503 (P = 0.0004; OR: 0.34; 95% CI: 0.19-0.64), and DRB5*010101 (P = 0.001; OR: 0.37; 95% CI: 0.20-0.67) were associated with susceptibility. The haplotype DRB1*1102-DRB3*020201 was associated with HIV-1 resistance (P = 0.041; OR: 1.68; 95% CI: 1.02-2.78), whereas the haplotypes DRB1*070101-DRB4*01010101 (P = 0.041; OR: 0.52; 95% CI: 0.28-0.98) and DRB1*1503-DRB5*01010101 (P = 0.0002; OR: 0.30; 95% CI: 0.15-0.58) were associated with susceptibility. These associations with resistance/susceptibility to HIV-1 were independent of previously reported alleles HLA-DRB1*01 and HLA-A*2301. CONCLUSION: Our findings indicate that human leukocyte antigen DRB-specific CD4+ T-cell responses are an important factor in resistance/susceptibility to HIV-1 infection.

Curr HIV/AIDS Rep. 2006 Feb;3(1):26-31

Understanding the "lucky few": the conundrum of HIV-exposed, seronegative individuals.

Shacklett BL.

Department of Medical Microbiology and Immunology, School of Medicine, University of California, Davis, 1 Shields Avenue, Davis, CA 95616, USA.

It has been known for many years that not all individuals who are repeatedly exposed to HIV-1 show evidence of viral replication, seroconvert, and eventually develop disease. Quite apart from those who seroconvert but progress slowly to AIDS (ie, slow progressors, long-term nonprogressors, elite controllers), these rare, exposed seronegatives either resist infection or harbor extremely low levels of virus that may be detected only using ultrasensitive methods (occult infection). The correlates of protection that confer this unique status to a tiny minority of HIV-exposed individuals remain a subject of intense interest, investigation, and controversy, as no single genetic or immunologic parameter has yet been able to fully explain this phenomenon. However, there is general consensus that studying these individuals may provide invaluable information to aid in the design of vaccines and therapeutic approaches. This review describes the major findings on this important topic, with a focus on immunologic studies.

Chin Med J (Engl). 2006 Oct 5;119(19):1616-21

Identification of HIV-1 specific T lymphocyte responses in highly exposed persistently seronegative Chinese.

Liu HW, Hong KX, Ma J, Yuan L, Liu S, Chen JP, Zhang YZ, Ruan YH, Xu JQ, Shao YM.

Division of Virology and Immunology, National Center for AIDS/STD Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing 100050, China.

BACKGROUND: Studies of highly exposed persistently seronegative (HEPS) individuals may provide valuable information on mechanisms of protection and on vaccine design. Cellular immune responses play a critical role in containing human immunodeficiency virus. However, the cellular immune responses in HEPS individuals have not been thoroughly assessed at the entire viral genome level. METHODS: Ten HEPS Chinese with a history of frequent penetrative vaginal intercourse (mean frequency, at least once a week), with some unprotected sexual contact occurring in the weeks or days immediately before enrollment, 25 HIV-1 seropositive individuals, 10 HIV-1-seronegative healthy individuals with low-risk sexual behavior and no history suggestive of exposure to HIV-1 infection were enrolled. HIV-1-specific T cell responses were comprehensively analyzed by an interferon-gamma Elispot assay against 770 overlapping peptides spanning all HIV-1 proteins. RESULTS: HIV-1-specific T-cell responses of interferon-gamma secretion were identified in 3 (30%) out of 10 HEPS individuals; the specific cytotoxic T lymphocytes were targeted at Pol (2/10), Env (2/10), and Tat (1/10). HIV-1-specific T-cell responses of interferon-gamma secretion were identified in 20 (80%) out of 25 seropositive intravenous drug users (IDUs), revealing that all HIV-1 proteins and protein subunits could serve as targets for HIV-1-specific CD8(+) T cell responses with 85% recognizing Gag, 80% recognizing Nef, 75% recognizing Pol, 60% recognizing Env, 55% recognizing Vpu, 45% recognizing Vpr, 20% recognizing Vif, 20% recognizing Tat and 15% recognizing Rev in these seropositive individuals. None of the seronegative healthy individuals gave the positive T-cell responses. CONCLUSIONS: About 30% of HEPS Chinese mounted HIV-1 specific T cell immune responses. Cell-mediated immunity against HIV-1 may be developed through non-productive infections.

Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 2006 Oct;28(5):613-7.

[Resistance to HIV-1 infection of CD4 + T lymphocytes in vitro from chinese HIV-1 exposed seronegative individuals]

[Article in Chinese]

Su YL, Shang H, Liu J, Wang SX, Geng WQ, Cui HL, Jiang YJ, Wang YN, Zhang ZN, Wang YT.
Center for AIDS Research, the First Affiliated Hospital, China Medical University, Shenyang 110001, China.

OBJECTIVE: To determine the relative resistance to HIV-1 infection of CD4 + T lymphocytes in HIV-exposed seronegative individuals (ESNs) in China. METHODS: HIV primary isolates were obtained from peripheral whole blood of HIV-infected persons. CD4 + T lymphocytes of Chinese ESNs were separated from peripheral blood mononuclear cells with magnetic cell sorting (MACS). The purified CD4 + T lymphocytes were cocultured with HIV primary isolates. The p24 level was detected and the culture medium was refreshed every 3 days within 2 weeks. RESULTS: For M tropic HIV strains, p24 level was significantly lower in ESN group than in control group (P 0.05). CONCLUSION: CD4 + T lymphocytes of Chinese ESNs may possess relative resistance to M tropic HIV strains, which may be one of the main influencing factors that result in ESN.

AIDS. 2006 Sep 11;20(14):1879-83.

CCR5 expression and duration of high risk sexual activity among HIV-seronegative men who have sex with men.

Thomas SM, Tse DB, Ketner DS, Rochford G, Meyer DA, Zade DD, Halkitis PN, Nádas A, Borkowsky W, Marmor M.

Department of Environmental Medicine, New York University School of Medicine, NY 10016-3240, USA

OBJECTIVES: To test the hypothesis that in comparison with those with shorter risk duration, individuals with longer HIV risk duration would have reduced susceptibility to HIV-1 infection as measured by CCR5 expression, and to evaluate whether variation in CCR5 expression could be explained by known genetic polymorphisms. DESIGN AND METHODS: A cross-sectional study of HIV-1 exposed but uninfected men who have sex with men. The risk duration was estimated from self-reported years since first receptive anal intercourse. CCR5 expression on peripheral blood CD4+ monocytes and T cells was determined by flow cytometry. The CCR5-Delta32 mutation and polymorphisms in the CCR5 promoter and CCR2 as well as the copy number of CCL3L1 were analyzed by polymerase chain reaction. Plasma levels of MIP-1alpha (CCL3), MIP-1beta (CCL4) and RANTES (CCL5) were also measured. As risk duration varied with age, analyses were restricted to 67 individuals aged 30-49 years. RESULTS: Multiple linear regression analyses, adjusted for age and race, showed a significant negative association between HIV risk duration and CCR5 expression on monocytes (P = 0.01), and in a separate model, a similar negative association with CCR5 expression on T cells (P = 0.03). Low CCR5 expression was attributable mainly to CCR5-Delta32 heterozygosity and the CCR5-59029G allele. CONCLUSIONS: We confirmed a role for reduced CCR5 expression in HIV-1 resistance. CCR5-Delta32 heterozygosity and the CCR5-59029G allele were significant predictors of low CCR5 expression. Individuals with high CCR5 expression who resisted infection despite long HIV risk duration form an interesting group within which to search for additional mechanisms of resistance to HIV infection.

J Clin Immunol. 2006 Sep;26(5):476-84. Epub 2006 Jul 25.

Gene polymorphisms in CCR5, CCR2, CX3CR1, SDF-1 and RANTES in exposed but uninfected partners of HIV-1 infected individuals in North India.

Suresh P, Wanchu A, Sachdeva RK, Bhatnagar A.

Department of Internal Medicine, Post Graduate Institute of Medical Education and Research, Chandigarh, India.

Repeated exposure to human immunodeficiency virus (HIV) does not always result in infection. Understanding the mechanisms that give protection against progressive infection with HIV may help in the development of a vaccine. In order to determine the influence of host genetic factors on HIV resistance, we studied 35 exposed but uninfected (EU) partners of HIV-1 infected individuals for polymorphisms in multiple chemokine and chemokine receptor genes and compared the results with those for 75 HIV-1 seronegative normal healthy controls (HC) and 50 HIV infected controls. There was no association between CCR5-Delta32, CCR2-64I, CX3CR1-280 M, CX3CR1-249I, SDF-3'A, RANTES-28G and RANTES-403A polymorphisms and susceptibility against HIV in our cohort of EU individuals. An increased frequency of SDF-1 3'A and RANTES-403A genotypes was present in EU individuals but the difference was not statistically significant when compared to healthy and HIV infected controls. These observations suggest that mechanisms other than genetic mutations of these genes might be responsible for resistance to HIV infection in these individuals.

J Acquir Immune Defic Syndr. 2006 Aug 1;42(4):412-9.

HIV-specific antibodies but not t-cell responses are associated with protection in seronegative partners of HIV-1-infected individuals in Cambodia.

Nguyen M, Pean P, Lopalco L, Nouhin J, Phoung V, Ly N, Vermisse P, Henin Y, Barré-Sinoussi F, Burastero SE, Reynes JM, Carcelain G, Pancino G.

Institut Pasteur du Cambodge, Phnom Penh, Cambodia.

To study biological factors related to protection against HIV-1 infection in Cambodia, we recruited 48 partners of HIV-1-infected patients who remained uninfected (exposed uninfected individuals, EUs) despite unprotected sexual intercourse for more than 1 year and 49 unexposed controls (UCs). HIV-1-specific antibodies (IgA anti-gp41 and IgG anti-CD4-gp120 complex), T-cell responses, and cellular factors that may be involved in protection (peripheral blood mononuclear cell [PBMC] resistance to HIV-1 infection and beta-chemokine production) were evaluated. Anti-HIV-1 antibodies were higher in EUs than those in UCs (P = 0.01 and P = 0.04 for anti-gp41 and anti-CD4-gp120, respectively). We observed a decreased susceptibility to a primary Cambodian isolate, HIV-1KH019, in EU PBMCs as compared with UC PBMCs (P = 0.03). A weak T-cell response to one pool of HIV-1 Gag peptides was found by ELISpot in 1 of 19 EUs. Whereas T-cell specific immunity was not associated to protection, our results suggest that HIV-specific humoral immunity and reduced cell susceptibility to infection may contribute to protection against HIV-1 infection in Cambodian EUs.

Zhonghua Shi Yan He Lin Chuang Bing Du Xue Za Zhi. 2006 Jun;20(2):72-4.

[Epidemiologic study and HLA analysis of highly exposed to HIV but persistently seronegative subjects (HEPS) in commercial blood donors in China]

[Article in Chinese]

Xu KY, Dong T, Lun WH.
Beijing Ditan Hospital, Beijing 100011, China.

BACKGROUND: To investigate epidemiology and HLA typing of highly exposed to HIV but persistently seronegative subjects (HEPS) in commercial blood donors in China. METHODS: This was a cohort study for epidemiologic characteristics of highly exposed but persistently seronegative subjects. PCR with sequence-specific primer and PCR-SSP for HLA typing were applied. RESULTS: Eight HEPS were identified. Compared HLA typing with seropositive couple, high frequency of HLA-a24, HLA-B40 genotyping was observed. CONCLUSION: Highly exposed to HIV but persistently seronegative subjects in commercial blood donors in China had high frequency of HLA-A24 and HLA-B40 genotype.

Virol J. 2006 Jun 29;3:52.

Human Immunodeficiency Virus type 1 in seronegative infants born to HIV-1-infected mothers.

Vázquez Pérez JA, Basualdo Sigales MC, Reyes-Terán G, Gudiño Rosales JC, Soler Claudín C.

Unidad de Servicios Para Diagnóstico y Referencia en VIH, Instituto de Investigaciones Biomédicas UNAM/Secretaría de Salud del DF, México D.F.

BACKGROUND: Some individuals repeatedly exposed to Human Immunodeficiency Virus do not seroconvert and are resistant to HIV infection. Here, in a pediatric cohort of HIV seronegative infants born of HIV-infected mothers, we have studied eight non-breastfed children in whom viral DNA was detected in their PBMC. Our objective was to assess whether silent infection in these children can be explained by the presence of integrated viral DNA. METHODS: The presence of viral DNA was corroborated by nested PCR with primers for gag and the nef/LTR regions of HIV-1. Integration of HIV DNA into the host genome was assessed by an Alu-LTR PCR. Amplicons were sequenced and phylogenetic analyzes were done. RESULTS: HIV-1 DNA was detected in the earliest available PBMC sample from all eight infants, and two of them tested positive for HIV DNA at 2 years of age. Nested PCR resulted in the amplification of gag, nef/LTR and Alu-LTR fragments, which demostrated that HIV-1 DNA was integrated in the host cell genome. Each individual has a characteristic sequence pattern and is different from the LTR sequence of HXB2 prototype virus and other Mexican isolates. CONCLUSION: HIV-1 DNA was observed in PBMC from HIV exposed seronegative children in this pediatric cohort.

J Immunol. 2005 Nov 1;175(9):6117-22.

Low-level CD4+ T cell activation is associated with low susceptibility to HIV-1 infection.

Koning FA, Otto SA, Hazenberg MD, Dekker L, Prins M, Miedema F, Schuitemaker H.
Department of Clinical Viro-immunology, Sanquin Research and Landsteiner Laboratory of the Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands.

Different features have been associated with low susceptibility to HIV type 1 (HIV-1) infection in exposed seronegative individuals. These include genetic make-up such as homozygosity for the CCR5-Delta32 allele and the presence of HIV-specific CTLs. We studied immune activation and immune responsiveness in relation to HIV-1 susceptibility in 42 high-risk seronegative (HRSN) participants of the Amsterdam Cohort Studies and 54 men from the same cohort who were seronegative at the moment of analysis but later became HIV seropositive. HRSN had higher naive (CD45RO CD27) CD4 and CD8 T cell numbers and lower percentages of activated (HLADR CD38, CD70) CD4 and proliferating (Ki67) CD4 and CD8 T cells, irrespective of previous episodes of sexually transmittable infections. Furthermore, whole blood cultures from HRSN showed lower lymphoproliferative responses than healthy laboratory controls. These data suggest that low levels of immune activation and low T cell responsiveness may contribute to low HIV susceptibility.

J Virol. 2005 Sep;79(18):11677-84.

Combined effect of CCR5-Delta32 heterozygosity and the CCR5 promoter polymorphism -2459 A/G on CCR5 expression and resistance to human immunodeficiency virus type 1 transmission.

Hladik F, Liu H, Speelmon E, Livingston-Rosanoff D, Wilson S, Sakchalathorn P, Hwangbo Y, Greene B, Zhu T, McElrath MJ.

Fred Hutchinson Cancer Research Center, Clinical Research Division, Program in Infectious Diseases, 1100 Fairview Ave. N., P.O. Box 19024, D3-100, Seattle, WA 98109-1024, USA.

Exposed seronegative individuals (ES) with persistent high-risk sexual behavior may be less susceptible to human immunodeficiency virus type 1 (HIV-1) infection because they carry the chemokine receptor (CR) gene alleles CCR5 open reading frame (ORF) Delta32, CCR5 promoter -2459G, or CCR2 ORF 64I (CCR2-64I), all of which have been found to diminish HIV-1 infectivity and/or disease progression. To investigate this, we determined the haplotypes for these three genetic loci in 93 ES and 247 low-risk control individuals. To test if protective haplotypes exert their effect by modulating CR expression, we measured the protein expression of CCR5 and CXCR4 on circulating CD4+ T cells and CD14+ monocytes in 71 ES and 92 controls. To avoid investigator bias, the analysis was performed without knowledge of each subject's risk and genotype. The CCR5 -2459G allele was significantly enriched in ES Caucasian men, who constituted the majority (84%) of the ES cohort, compared to the control Caucasian men (P = 0.02). This increase was mostly attributable to a higher frequency of the -2459 A/G versus the -2459 A/A genotype in individuals heterozygous for the delta32 allele (P = 0.012). No protective influence of the CCR2-64I allele was observed. The haplotypes CCR5 ORF delta32/CCR5 -2459A (in complete linkage disequilibrium) and CCR5 ORF wt/CCR5 -2459G had a cumulative negative effect on the expression of CCR5, since we measured significantly reduced CCR5 densities on both T-helper cells and monocytes only when both haplotypes were present. Densities of CCR5 on lymphocytes and monocytes were correlated (r = 0.59; P

Virol J. 2005 Aug 17;2:65.

Evidence of HIV exposure and transient seroreactivity in archived HIV-negative severe hemophiliac sera.

Tenenbaum SA, Morris CA, Alexander SS, McFerrin HE, Garry RF, Leissinger CA.
Department of Biomedical Sciences, Ge*NY*Sis Center for Excellence in Cancer Genomics, University at Albany-SUNY, Albany, NY, USA.

BACKGROUND: Approximately 25% of hemophiliacs that were frequently exposed to blood clotting factor concentrates (CFCs) contaminated with human immunodeficiency virus (HIV) are presently HIV seronegative. In this study, we sought to determine if some of these individuals were at any time transiently HIV seropositive. In the early to mid-1980s the majority of severe hemophilia patients were exposed to CFCs contaminated with HIV. Although many of these hemophiliacs became HIV-positive, a small percentage did not become infected. To determine if some of these individuals successfully resisted viral infection, we attempted to document the presence of transient HIV reactive antibodies in archived plasma samples (1980-1992) from currently HIV-negative severe hemophiliacs who had a high probability of repeated exposure to HIV contaminated CFC. Archived plasma samples were retrospectively tested using an FDA approved HIV-1Ab HIV-1/HIV-2 (rDNA) enzyme immunoassay (EIA) and a HIV-1 Western blot assay (Wb), neither of which were commercially available until the late 1980s, which was after many of these samples had been drawn. RESULTS: We found that during the high risk years of exposure to HIV contaminated CFC (1980-1987), low levels of plasma antibodies reactive with HIV proteins were detectable in 87% (13/15) of the haemophiliacs tested. None of these individuals are presently positive for HIV proviral DNA as assessed by polymerase chain reaction (PCR). CONCLUSION: Our data suggest that some severe hemophiliacs with heavy exposure to infectious HIV contaminated CFC had only transient low-level humoral immune responses reactive with HIV antigens yet remained HIV-negative and apparently uninfected. Our data supports the possibility of HIV exposure without sustained infection and the existence of HIV-natural resistance in some individuals.

J Virol. 2005 May;79(10):6551-3.

Low levels of human immunodeficiency virus type 1 DNA in high-risk seronegative men.

Koning FA, van der Vorst TJ, Schuitemaker H.

Sanquin Research at CLB, Dept. of Clinical Viro Immunology, Plesmanlaan 125, 1066 CX Amsterdam, The Netherlands.

We detected human immunodeficiency virus type 1 (HIV-1) DNA at very low levels in sequential peripheral blood mononuclear cell samples of five out of six high-risk, seronegative, homosexual men and five out of five individuals 7.8 to 1.6 years prior to seroconversion. These data indicate a high prevalence of low-level HIV-1 DNA in exposed seronegative individuals.

AIDS. 2005 Apr 29;19(7):653-61.

Distinct patterns of HIV-specific memory T lymphocytes in HIV-exposed uninfected individuals and in HIV-infected patients.

Schenal M, Lo Caputo S, Fasano F, Vichi F, Saresella M, Pierotti P, Villa ML, Mazzotta F, Trabattoni D, Clerici M.

Immunology DISP LITA Vialba, University of Milano, Milano, Italy.

BACKGROUND: Repeated exposure to HIV is not always associated with infection and multiple cohorts of HIV-exposed but seronegative individuals (ESN) have been described. HIV-specific CD4 and CD8 T lymphocytes are detected both in HIV patients and in ESN; we verified whether different patterns of HIV-specific memory T lymphocytes would be detected in individuals in whom exposure to HIV results or does not result in infection. METHODS: Gag-specific T cells were analysed in 15 ESN, 14 HIV patients, and 15 healthy controls using extensive flow cytometry analysis. RESULTS: Data confirmed that gag-specific T lymphocytes are present in ESN. Gag-specific T cells mainly secrete interleukin-2 in ESN and interferon-gamma in HIV patients. In addition the CD4/CD8 and the memory/naive ratios are altered, central memory (45RA-/CCR7+) CD4 and CD8 T lymphocytes are more abundant, and terminally differentiated (45RA+/CCR7- and 27-/28-) CD8 T lymphocytes are augmented in ESN individuals. CONCLUSIONS: Exposure to HIV occurs in high risk seronegative individuals; the observation that naive cells and CM are skewed in ESN indicate that this exposure is robust enough to modulate the CM/EM ratio. The increase in late effectors and in natural killer cells seen in ESN suggests a role for these cells in preventing actual infection.

J Infect Dis. 2005 Jan 1;191(1):20-4. Epub 2004 Dec 1.

CD4+ T cell responses in HIV-exposed seronegative women are qualitatively distinct from those in HIV-infected women.

Alimonti JB, Koesters SA, Kimani J, Matu L, Wachihi C, Plummer FA, Fowke KR.
Department of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg, Manitoba R3E 0W3, Canada.

The immune response of human immunodeficiency virus (HIV)-exposed seronegative (ESN) women may be qualitatively different from that in those infected with HIV (HIV(+)). In a cohort of female commercial sex workers in Nairobi, Kenya, we found significantly lower (P

Immunol Res. 2004;29(1-3):161-74.

Insights into the role of host genetic and T-cell factors in resistance to HIV transmission from studies of highly HIV-exposed Thais.

McNicholl JM, Promadej N.

Immunogenetics Section, HIV Immunology and Diagnostics Branch, National Center for HIV, STD and TB Prevention, Centers for Disease Control and Prevention, 1600 Clifton Road NE, Atlanta, GA 30333, USA.

Studies of resistance to HIV-1 transmission are likely to be valuable for the design of vaccines and other efforts to prevent HIV. Here, we review the T-cell and genetic factors associated with resistance to HIV-1 transmission in studies of highly exposed but persistently seronegative (HEPS) women from northern Thailand. Women were enrolled in two sex-worker studies and in a discordant couple study. We performed Cr51 cytotoxic T lymphocyte (CTL), interferon-gamma (IFN-gamma) ELISPOT, and proliferation assays as well as genetic studies, including HLA-class I typing. CTL and ELISPOT studies showed a skewing of T-cell responses to conserved HIV-1 proteins in HEPS, but not in HIV-1-seropositive women. T-cell responses were extremely long-lived in some HEPS women. In the two sex-worker studies, HLA-A11 was associated with resistance to HIV-1 transmission. These data provide promise for the ability of CTL to control HIV and emphasize the importance of developing HIV vaccines that stimulate strong, long-lasting Tcell responses.

AIDS. 2004 May 21;18(8):1117-26.

Correlates of resistance to HIV-1 infection in homosexual men with high-risk sexual behaviour.

Koning FA, Jansen CA, Dekker J, Kaslow RA, Dukers N, van Baarle D, Prins M, Schuitemaker H.

Department of Clinical Viro Immunology, Sanquin Research at CLB and Landsteiner
Laboratory of the Academic Medical Centre, University of Amsterdam, The Netherlands.

OBJECTIVE: To investigate possible correlates of HIV resistance in participants from the Amsterdam Cohort of Homosexual men who have remained HIV seronegative despite high-risk sexual behaviour. DESIGN/METHODS: We studied in vitro HIV-1 susceptibility and adaptive and innate immunity in 29 high-risk seronegative (HRSN) and 15 HIV-negative pre-seroconversion (pre-SC) homosexual men from the same Amsterdam Cohort Study (ACS) who seroconverted to HIV-1 positive during active follow-up. Host genetics were compared between HRSN and HIV-positive ACS participants. RESULTS: We found lower in vitro susceptibility for a CCR5-using (R5) HIV-1 variant, higher RANTES production levels, but no difference in coreceptor expression in HRSN as compared with pre-SC controls. Reduced R5 in vitro susceptibility of two HRSN tested was restored to normal levels by addition of antibodies against beta-chemokines. A higher proportion of HRSN carried the SDF-1 3'A variant and HLA-A*11, A*31 and Cw*15 alleles. ELIspot analysis with HIV-1 peptide stimulation revealed low frequencies of HIV-1-specific CD8 interferon-gamma producing cytotoxic T cells in both HRSN and pre-SC controls. CONCLUSIONS: Low in vitro R5 susceptibility of cells from the HRSN men was due to beta-chemokine mediated inhibition of virus replication. The presence of HIV-1 specific cytotoxic T cells in both HRSN and pre-SC participants may signify exposure to the virus rather than protection from infection. Host genetic characteristics and other factors affecting innate immunity may contribute to differential resistance to HIV-1 infection among exposed seronegative individuals.

J Infect Dis. 2004 May 1;189(9):1705-13. Epub 2004 Apr 19.

Distinct patterns of peripheral HIV-1-specific interferon- gamma responses in exposed HIV-1-seronegative individuals.

Kebba A, Kaleebu P, Rowland S, Ingram R, Whitworth J, Imami N, Gotch F.
Department of Immunology, Imperial College, London, Chelsea and Westminster Hospital, London, United Kingdom.

It is unclear how human immunodeficiency virus (HIV) type 1-specific immune responses in exposed seronegative (ESN) individuals differ from those in HIV-1-infected subjects. By use of overlapping peptides spanning Gag, Tat, Nef, Vif, Vpr, and Vpu, peripheral blood mononuclear cells from ESN individuals, their seropositive (SP) partners, and unexposed seronegative control subjects were screened for interferon- gamma production. Responses were more frequent (95.7% vs. 20%), of a higher magnitude (9-fold), and of wider breadth (median number of peptides recognized, 18 vs. 2.5) in SP than in ESN individuals. Peptides recognized by ESN individuals were less frequently recognized by their SP partners. SP subjects infrequently recognized peptides from Vif, and such responses were subdominant; among ESN individuals, this HIV-1 protein was most frequently recognized. Immunodominant peptides recognized by SP subjects tended to be from relatively conserved regions, whereas peptides recognized by ESN individuals were associated with slow disease progression.

AIDS Res Hum Retroviruses. 2004 Jan;20(1):67-75.

HIV type 1 antigen-responsive CD4+ T-lymphocytes in exposed yet HIV Type 1 seronegative Ugandans.

Kebba A, Kaleebu P, Serwanga J, Rowland S, Yirrell D, Downing R, Gilmour J, Imami N, Gotch F, Whitworth J.

Medical Research Council's Programme on AIDS in Uganda, UVRI, Entebbe, Uganda.

CD4(+) T cell help is important for the functionality of CD8(+) cytotoxic T-lymphocytes (CTLs) in limiting viral replication and may contribute to mediation of apparent resistance to HIV-1 infection in exposed seronegative (ESN) individuals. Using five HIV-1 antigens in an intracellular cytokine assay, the presence of specific antigen-responsive interferon- gamma-positive (IFN-gamma(+)) CD69(+) CD4(+) T-lymphocytes was evaluated in ESNs, their seropositive partners, and unexposed seronegative controls. Ten ESNs (five females, five uncircumcised males) were identified from 10 HIV-1 serodiscordant couples with a history of frequent unprotected sexual intercourse. All ESNs and controls were negative on two EIAs and for HIV-1 proviral DNA. The frequency of ESNs with antigen-responsive IFN-gamma(+) CD69(+) CD4(+) T-lymphocytes ranged from three to five of eight for the different HIV-1 antigens. Six of eight ESNs tested had a positive response to at least one of the five antigens. Responses were on average 3.5 times higher among seropositives compared to ESNs and absent in the five unexposed controls. A negative correlation was noted between responses in ESNs and the plasma viral load of their seropositive spouse. Clade-specific and cross-clade reactivity were noted in both ESNs and seropositive partners tested. The findings confirm that ESNs are in a state of HIV-1-specific immune activation and suggest that HIV-1-specific IFN-gamma(+) CD69(+) CD4(+) T-lymphocytes in addition to HIV-1-specific CD8(+) CTLs already described by others are potential immunological correlates of protection from persistent HIV-1 infection.

J Infect Dis. 2004 Feb 15;189(4):602-10. Epub 2004 Jan 29.

HIV-specific T helper responses and frequency of exposure among HIV-exposed seronegative female sex workers in Abidjan, Cote d'Ivoire.

Jennes W, Vuylsteke B, Borget MY, Traore-Ettiegne V, Maurice C, Nolan M, Nkengasong JN, Kestens L.

Department of Microbiology, Laboratory of Immunology, Institute of Tropical Medicine, Nationalestraat 155, 2000 Antwerp, Belgium.

BACKGROUND: The characteristics of human immunodeficiency virus (HIV) exposure that determine the induction of HIV-specific T cells and, in particular, T helper cells are not well understood. METHODS: HIV-1 Gag- and Env-specific T helper cells were analyzed by use of an interferon (IFN)- gamma enzyme-linked immunosorbent spot (ELISPOT) assay and by use of IFN- gamma secretion flow cytometry. Responses among HIV-exposed seronegative (ESN) female sex workers (FSWs) were compared with responses among HIV-seropositive FSWs and HIV-seronegative female blood donors from Abidjan, Cote d'Ivoire. RESULTS: Low-level ELISPOT responses were detected in 8 (20%) of 40 ESN FSWs. All of 25 HIV-seropositive FSWs had high-level ELISPOT responses. HIV-specific CD4+ T cells and, occasionally, CD8+ T cells were detected by secretion flow cytometry in 3 (38%) of 8 ESN FSWs and in 4 (80%) of 5 HIV-seropositive FSWs. ESN FSWs with detectable HIV-specific T helper responses had more clients on the previous working day (P=.02) and more exposures to HIV per month (P=.02) and tended to have a lower total duration of commercial sex work. CONCLUSIONS: These findings demonstrate that the presence of HIV-specific T helper cells in ESN FSWs is associated with the frequency, rather than the duration, of exposure to HIV. The data may have important implications for the evaluation of HIV vaccine efficacy.

AIDS. 2003 Nov 7;17(16):2299-311.

Evidence for Gag p24-specific CD4 T cells with reduced susceptibility to R5 HIV-1 infection in a UK cohort of HIV-exposed-seronegative subjects.

Eyeson J, King D, Boaz MJ, Sefia E, Tomkins S, Waters A, Easterbrook PJ, Vyakarnam A.
Department of Immunology, Guy's, King's and St Thomas' School of Medicine and Dentistry, King's College Hospital, London SE5 9NU, UK.

AIM: To characterize HIV-1 Gag p24-specific CD4 cell responses in HIV-exposed-seronegative (ES) individuals. METHODOLOGY: Twelve ES individuals, of diverse ethnicity and wild type for the CCR5 Delta-32 mutation, were identified. Controls were HIV-negative blood donors. Gag p24-specific and total Vbeta+ CD4 cells that expressed MIP-1beta, IFN-gamma and IL-2 were enumerated by intracytoplasmic cytokine staining. beta-Chemokine expression was correlated with susceptibility to R5 HIV-1 infection, as measured by polymerase chain reaction for integrated HIV-1 and by p24 enzyme-linked immunosorbent assay. RESULTS: Similar numbers of mitogen-stimulated and Vbeta+ MIP-1beta+, IFN-gamma+ and IL-2+ T cells were found in ES and HIV-negative control subjects. However, all ES subjects tested had an HIV Gag p24-specific MIP-1beta+, IFN-gamma+ and IL-2+ CD4 T-cell response that was rare in controls. p24-Specific cells of all ES but no control subjects could be expanded by in-vitro Ag/IL-2 stimulation, and when re-stimulated with an overlapping peptide series showed evidence of a broad CD4 cell memory response directed against multiple regions of Gag p24. Mitogen-stimulated ES CD4 cells were as susceptible to HIV infection as those from control subjects, but p24-specific IFN-gamma+ CD4 cells of six out of seven ES subjects tested were less susceptible to R5 HIV-1 infection than the counterpart fraction depleted of p24-specific IFN-gamma+ cells. The addition of blocking anti-beta-chemokine antibodies did not promote R5 HIV-1 infection of p24-specific IFN-gamma+ cells. CONCLUSION: Specific CD4 cell immunity, characterized by a broadly directed memory Gag-p24 CD4 cell response and reduced susceptibility of specific CD4 cells to R5 HIV-1 infection, is a likely correlate of non-transmission.

AIDS Res Hum Retroviruses. 2003 Aug;19(8):661-5.

Polymorphisms in the CCR5 coding and noncoding regions among HIV type 1-exposed, persistently seronegative female sex-workers from Thailand.

Yang C, Li M, Limpakarnjanarat K, Young NL, Hodge T, Butera ST, McNicholl JM, Mastro TD, Lal RB.

HIV Immunology and Diagnostics Branch, Division of AIDS, STD, and TB Laboratory Research, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, Atlanta, GA 30333, USA.

Resistance to HIV-1 infection despite repeated exposures has been associated with one or more HIV-specific responses, enhanced nonspecific immune modifications, and/or host genetic polymorphisms in certain individuals (highly exposed, persistently seronegative, HEPS). In the present investigation, we focused on the CCR5 gene polymorphisms and the association of such mutations to resistance to HIV-1 infection among 12 HEPS women in Chiang Rai, northern Thailand, and compared our findings with data from 10 HIV-1-infected and 9 HIV-1-uninfected unexposed women from the same geographic area. Although we have previously shown that none of the Thai women carried the Delta32 mutation, further analysis of the CCR5 coding gene region revealed that none of the women had other mutations that affect coreceptor activity (C101X or FS299) or chemokine responses (C20S, A29S, L55Q, C178R). Analysis of the CCR5 promoter region revealed that the CCR5 haplogroup C (HHC; 60%) was the predominant haplogroup among these women. Comparative analysis of the frequencies of different haplogroups among the three groups did not reveal any statistically significant differences (p 0.05). However, we did find that two individuals from the HEPS group were homozygous for HHF*2 (the CCR2b- 64I bearing haplogroup) compared to none from the HIV-1-infected and -uninfected groups. There was no detectable difference in specific CCR5 haplogroups and their ability to mediate env fusion or to mediate HIV-1 infection in vitro. These data suggest that homozygosity of the HHF*2 haplogroup may be one of the factors that mediate resistance to HIV-1 infection in this cohort of HEPS women.

AIDS Rev. 2003 Apr-Jun;5(2):87-103.

Resistance to HIV-1 infection: lessons learned from studies of highly exposed persistently seronegative (HEPS) individuals.

Kulkarni PS, Butera ST, Duerr AC.

HIV and Retrovirology Branch, National Center for Infectious Diseases, Centers for Disease Control and Prevention, 1600 Clifton Road, NE, Atlanta, GA 30333, USA.

The medical, social, and economic impact of the human immunodeficiency virus (HIV) epidemic has underscored the need to quickly develop effective control strategies. Vigorous efforts to develop a vaccine and therapeutic agents have not yet succeeded in containing the spread of the virus. Studies of persons who remain uninfected despite extensive exposure to HIV continue to provide valuable information on mechanisms of natural protection, which can then be applied to vaccine design. Natural resistance to infection has been studied in multiple high-risk cohorts, with resistance attributed to a combination of innate, genetic, and acquired immune system-mediated mechanisms. The relative contributions of these factors to natural resistance to HIV-1 infection and possible ways in which they can be applied to vaccine design are discussed.

J Virol. 2003 Jun;77(11):6108-16.

Persistence of extraordinarily low levels of genetically homogeneous human immunodeficiency virus type 1 in exposed seronegative individuals.

Zhu T, Corey L, Hwangbo Y, Lee JM, Learn GH, Mullins JI, McElrath MJ.

Department of Laboratory Medicine, University of Washington School of Medicine, Seattle 98195, USA.

Some individuals remain inexplicably seronegative and lack evidence for human immunodeficiency virus type 1 (HIV-1) infection by conventional serologic or virologic testing despite repeated high-risk virus exposures. Here, we examined 10 exposed seronegative (ES) individuals exhibiting HIV-1-specific cytotoxicity for the presence of HIV-1. We discovered HIV-1 DNA in resting CD4(+) T cells (mean, 0.05 +/- 0.01 copies per million cells) at multiple visits spanning 69 to 130 weeks in two ES individuals at levels that were on average 10(4)- to 10(6)-fold lower than those of other HIV-1-infected populations reported. Sequences of HIV-1 envelope and gag genes remained markedly homogeneous, indicating little to undetectable virus replication. These results provide the evidence for HIV-1 infection in ES individuals below the detection limit of standard assays, suggesting that extraordinary control of infection can occur. The two HIV-infected ES individuals remained healthy and were not superinfected with other HIV-1 strains despite continued high-risk sexual exposures to multiple HIV-infected partners. Understanding the mechanisms that confer diminished replicative capacity of HIV-1 in these hosts is paramount to developing strategies for protection against and control of HIV-1 infection.

Here are some sources to look through obtained from another discussion of this. I'm not sure what your background is so these results were obtained with the term: HIV exposed seronegative. What Luc Montagnier talked about is no secret. He has said the same thing since 1992. This in no way supports AIDS denialism. Montagnier never has claimed that HIV is not the cause of AIDS or that a healthy immune system alone will render HIV negligible. He has maintained that HIV is necessary for the AIDS virus to develop but maintains there is more to the picture that we are missing. Other studies(including those contained in the spoiler) will show that the idea that HIV can only lead to AIDS in a malnourished immune system is inexplicably incorrect.

I realize that you are not taking a position of AIDS denialism but I felt it was important to stress these points.