• We are sorry, but NCBI web applications do not support your browser and may not function properly. More information
Logo of nihpaAbout Author manuscriptsSubmit a manuscriptNIH Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Antivir Ther. Author manuscript; available in PMC Apr 8, 2010.
Published in final edited form as:
Antivir Ther. 2009; 14(6): 731–738.
doi:  10.3851/IMP1253
PMCID: PMC2851194
NIHMSID: NIHMS188582

Host genome influences on HIV-1 disease

Abstract

HIV host genetics seeks to describe as comprehensively as possible the impact of human genetic variation on the individual response to HIV-1 infection. Many associations between specific gene variants and HIV-1 disease outcomes have been reported over the past 15 years. While most of them have yet to be confirmed or were proven false positives, the identification of several definitive genotype-phenotype associations has shed new light on HIV-1 pathogenesis. This review discusses these results in the context of the new genome-wide approaches that now make it possible to globally assess the influence of the host genome on HIV-related outcomes.

Differences between individuals exposed to the HIV-1 virus have been observed since the early days of the current pandemic. Susceptibility to HIV-1 infection and natural history of the disease are highly variable, owing to the complex interplay between the virus, its human host, and the environment. Over the past 20 years, research in HIV host genetics has unraveled a series of human gene variants that modulate the response to retroviral exposure [1-3], thereby partially explaining why some individuals remain uninfected even when repeatedly exposed to HIV-1, or why a subset of infected patients are able to maintain a normal level of immunity after years of infection.

Most of the discoveries to date resulted from candidate gene studies, in which allelic variants have been analyzed in genes that were known or suspected to play a role in HIV-1 pathogenesis and immune response. As a consequence, the genetic markers relevant to HIV-1 disease that have been identified so far are related to genes that can broadly be classified into one of these 2 categories: (1) host genes that are implicated in HIV-1 life cycle, from entry into the target cells to the different intracellular steps that are required for viral replication and propagation; (2) immune-related genes, coding for canonical innate and adaptive immune response factors, as well as for proteins involved in immune-regulation and in specific antiretroviral defense mechanisms.

This review will summarize the known host genetic associations with HIV-1 outcomes, and put this knowledge in the context of the current genomic era. Indeed, the availability of genome-wide approaches represent a change in paradigm for complex trait genetic studies: global host influences on HIV can now be assessed in single experiments, and individual contributions of numerous genetic variants can be ranked and compared to get a comprehensive view of the impact of human genomic variation on HIV-1 infection [4].

HIV Life cycle

a. Entry: chemokine receptors

The only genetic variants that have been consistently associated with protection against HIV-1 acquisition are affecting the CC chemokine receptor 5 (CCR5) gene, which encodes the main co-receptor for macrophage-tropic (or R5) strains of HIV, normally expressed on CD4 T cells. A number of polymorphisms located in the coding and the promoter regions of the CCR5 gene have been found to associate with HIV-related outcomes. Most notably, a 32 base pair deletion (Δ32) in the CCR5 coding region results in the production of a truncated protein that is not expressed on the cell membrane. The CCR5 Δ32 variant affords protection against infection by R5 viruses in individuals who are homozygous for this allele, and slows down disease progression in heterozygotes [5-8]. Several other uncommon genetic variants of the CCR5 coding region have been described in individuals from various human populations [9-12], but their impact on HIV co-receptor function has not been completely established, except for the rare CCR5 303T>A change (also referred to as m303 or C101X) that introduces a premature stop codon and thus prevents functional co-receptor expression. This mutation was able to entirely block entry of R5 HIV-1 into its target cell in vitro [11]; the combination of m303 heterozygosity and the Δ32 deletion on the other allele confers resistance to HIV-1 infection [13]. Both Δ32 and m303 are found exclusively in patients of European ancestry, with minor allele frequencies of 10% and 0.2%, respectively.

Promoter variants of the CCR5 gene have been reported that influence the pace of progression to AIDS. By modulating the expression of CCR5, they can have an impact on cellular susceptibility [14]. The so-called HHE haplotype, which carries the previously reported P1 variant, associates with increased CCR5 expression and faster disease progression [15-17].

A Valine to Isoleucine change in the CCR2 gene (CCR2-64I variant) has been shown to delay progression to AIDS in a dominant way [18]. The frequency of CCR2-64I does not vary much between populations, with an average frequency of 10 to 20%. Since CCR2 is only a minor co-receptor that HIV-1 does not directly use for host cell entry in vivo, and because the V64I substitution is conservative, it is not entirely clear how the 64I allele exerts its protective effect: one proposed explanation is that the 64I allele acts on CCR2 splicing variants that result in down-modulation of CCR5 expression [19], but other studies failed to show an association between CCR2 variation and CCR5 expression levels [20, 21].

Variants of the chemokine receptors CX3CR1, CXCR1 (IL8RA) and CXCR6 have been reported to associate with various HIV outcomes [22-26], but none of these associations could yet be convincingly replicated. More recently, a report suggested that a variant in the Duffy antigen/receptor for chemokines (DARC) modulates HIV susceptibility [27]. DARC is a non-specific chemokine receptor that binds many inflammatory chemokines but lacks the ability to signal upon ligand binding; it is also the receptor for Plasmodium vivax. A −46T>C promoter polymorphism entirely suppresses DARC expression in red blood cells and confers resistance to vivax malaria. Homozygosity for the null allele (−46C) was therefore strongly enriched in regions affected by this pathogen: this allele is nearly fixed in sub-Saharan African populations, while the functional allele (−46T) is fixed in European populations. He et al. reported that HIV-infected African Americans have a frequency of the null homozygous genotype of 70% while HIV-negative individuals have a frequency of 60%. Therefore, they argued that DARC −46C/C increases susceptibility to infection [27]. Interestingly, in the same study, the null genotype associated with slower disease progression if infection occurred.

b. Entry: chemokines

Chemokines are natural ligands for the same receptors that HIV-1 uses to enter the cells. They can therefore have an impact on HIV-1 entry into host target cells by two means: they compete with the virus for co-receptor binding and/or they reduce the expression of the co-receptors on the cell surface by inducing their internalization. Regulated on activation normal T-cell expressed and secreted protein (RANTES), Macrophage inflammatory proteins (MIP1α and MIP1β), and stroma-derived factor (SDF-1) are examples of human chemokines that have polymorphisms in their coding genes that have been reported to play a role in differential susceptibility to HIV-1.

The CC-chemokine RANTES, encoded by the CCL5 gene, potently inhibits HIV-1 replication in vitro [28]. In vivo, decreased expression of RANTES was shown to accelerate progression whereas the opposite effect was observed with RANTES upregulation [29]. Several polymorphisms located in regulatory regions of CCL5 have been grouped in haplotypes that appear to modulate gene expression and as a consequence associate with differences in HIV-1 susceptibility and disease progression [30-34].

Several other CC-chemokine genes have been scrutinized in many HIV host genetic studies. Polymorphisms in the coding and non-coding regions of the CCL3 gene (MIP1α) have been shown to associate with both resistance and progression [32, 35]. More recently, it was shown that multiple copies of the CCL3L1 gene (MIP1αP) associate with resistance to HIV infection and with slower disease progression [36, 37], presumably through modulation of CCL3L1 expression. Analyses of the CCL2-CCL7-CCL11 gene cluster revealed variants that lead to differences in susceptibility to infection [38-40]. Here again, an increase in chemokine expression is proposed as the causal mechanism: notably, a CCL2 promoter polymorphism (−2578G) that associates with a reduced risk of acquiring HIV-1 was shown to increase CCL2 protein expression due to differential binding of the transcription factor IRF-1 to the polymorphic region [41].

SDF-1 is the natural ligand for CXCR4, the co-receptor for HIV-1 X4 strains. Many publications have looked at variation of the SDF-1 gene (CXCL12) and its relevance to HIV-1 pathogenesis: in particular, a variant located in the 3′-untranslated region of the gene (SDF-1 3′A) was reported to have various effects on progression [16, 42-45]. However, no convincing evidence could finally emerge from a large meta-analysis [46] and the importance of SDF-1 variation is still controversial.

c. Intracellular life cycle

Inside its target cell, HIV-1 interacts with numerous host proteins: some act as antiviral factors (see ‘intrinsic immunity’ below), but most of them are necessary for sustaining viral replication: HIV-1 has the capacity to hijack numerous human proteins in order to successfully complete its life cycle, as demonstrated in several recent large-scale siRNA screens [47-49]. Since human genes that act as HIV-1 co-factors represent ideal candidate genes, many of them have been investigated in host genetic studies. However, only two such genes have variants that were shown to play a role in the modulation of HIV pathogenesis and were confirmed in subsequent studies: tumor susceptibility gene 101 (TSG101) and peptidyl propyl isomerase A (PPIA, encoding the cyclophilin A protein).

The TSG101 protein interacts with the P6 product of HIV-1 Gag and is known to be critical in the budding process of new viral particles from the plasma membrane of infected cells: haplotypes constructed from 2 polymorphisms located in the 5′-region of the gene (−183T>C and +181A>C) were shown to influence multiple outcomes, including viral load and disease progression measured by CD4 T-cell decrease [44, 50]. The cyclophilin A protein is incorporated into the HIV-1 virion as a result of an interaction with the viral capsid protein: the mechanism by which cyclophilin A is able to enhance HIV-1 infection is still largely unknown, even if it has been suggested that it is involved in the uncoating of the viral core [51] and can also act as a cofactor for the anti-HIV TRIM5 protein [52]. Several variants located in regulatory regions of the PPIA gene have been shown to influence CD4 T-cell depletion and possibly susceptibility to infection [44, 53, 54].

d. Intrinsic antiretroviral factors

In addition to those host proteins that are necessary for HIV-1 to efficiently replicate, the human genome encodes molecules that have an antiretroviral function: most notably, TRIM5α and APOBEC3G have both been shown to be potent inhibitors of retroviral replication.

TRIM5α restricts HIV-1 at a postentry, preintegration stage in the viral life cycle, by recognizing the incoming retroviral capsid and promoting its premature disassembly. This inhibition process is species-specific: in fact, the capacity of human TRIM5α to inhibit HIV-1 replication is limited, whereas its simian ortholog restricts the human virus very efficiently. In vitro experiments have shown that several polymorphisms in the human TRIM5α gene correlate with differences in antiretroviral potency, but most the in vivo data suggest that common human variants of TRIM5α have no effect or only modest influence on HIV-1 disease outcomes [55-58].

APOBEC3G was first identified as a cellular factor able to restrict replication of HIV-1 viruses lacking the accessory protein Vif [59]. Its cytidine deaminase activity impacts viral replicative capacity by introducing G to A hypermutations in the HIV-1 DNA. An H186R coding change observed mainly in African populations was reported to associate with accelerated progression to AIDS, even if the in vitro antiviral activity of the 186R enzyme was not inferior to that of the common H186 variant [60]. A thorough analysis of APOBEC3G polymorphisms in Caucasians did not show any association with HIV-1 control [61]. Here again, larger studies in ethnically-controlled populations are warranted.

Immunity

a. Human leukocyte antigens

The most prominent and consistent associations identified in HIV host genetic studies are those between Human Leukocyte Antigen (HLA) genes and disease outcomes. Three genes (HLA-A, HLA-B, HLA-C) encode the HLA Class I proteins. Fundamental to the adaptive immune response, HLA molecules are expressed at the cell surface where they present antigenic epitopes and notably viral peptides to CD8+ T cells, thereby initiating a cytotoxic T cell response.

The HLA Class I genes present an extreme allelic diversity and are in fact the most polymorphic genes in the human genome. Once a particular individual gets infected by HIV-1, the potency of the elicited immune response depends on the retroviral epitopes that his HLA alleles are able to present to CD8+ T cells. The HLA allele that most consistently associates with potent control of HIV-1 is B*57 [62-64], with B*5701 observed almost exclusively in Caucasians and B*5703 mostly seen in individuals of African ancestry. Of note, a single nucleotide polymorphism that is a proxy for HLA-B*5701 showed one of the strongest association with HIV-1 viral control or long-term non-progression in all 3 genome-wide association studies published to date in the HIV field [64-66]. There is also clear epidemiological and functional evidence for effective restriction of HIV-1 by HLA-B*27 [67, 68]. In contrast, HLA-B*35Px (including B*3502, B*3503, B*3504 and B*5301) associates with faster progression to AIDS [69, 70]. Several haplotypes in the Major Histocompatibility Complex (MHC) and various HLA supertypes have been implicated in HIV-1 control [71-75], but most of the associations are likely to be due to individual alleles that are included in these groups and to the long-range linkage disequilibrium structure of the MCH region.

Thus, HLA molecules have the ability to present different HIV-1 epitopes, which result in variable restriction of the virus by the CD8+ T cells. Yet, this is not the only way the MHC region contributes to the inter-individual differences observed in HIV pathogenesis: homozygosity for HLA-A, HLA-B and/or HLA-C reduces the repertoire of antigen presentation, limits the number of epitopes recognized by CTLs and results in a faster disease progression [70, 76]. Additionally, while most of the associations with HIV-1 outcomes identified in the MHC region involve the HLA-B gene, there is some evidence that the importance of genetic variation in HLA-C may have been underestimated [77]: a genome-wide association study of determinants of HIV-1 viremia in seroconverters identified a polymorphism in the 5′ region of HLA-C that associates with both viral control and expression of the gene [64], suggesting that the amount of available HLA Class I molecules can also play a role in the efficacy of the immune response.

b. Killer cell immunoglobulin-like receptors

In addition to their importance for acquired immunity processes, HLA molecules are also ligands for the killer cell immunoglobulin-like receptors (KIR). The KIR receptors are preferentially expressed at the surface of the natural killer cells (NK) and regulate their activation status through inhibitory or activating signaling. NK cells represent an essential innate immune defense mechanism against viruses, being able not only to kill infected cells but also to produce cytokines.

Certain HLA-KIR combinations have epistatic influences on the outcome of HIV infection [78]: KIR3DL1 and KIR3DS1, which are expressed as allelic variants of the same locus on chromosome 19, have both been shown to protect against disease progression when found in combination with HLA-B molecules that have a Bw4 serologic specificity. Various combinations of inhibitory KIR3DL1 alleles and HLA Bw4 molecules have been associated with lower HIV-1 viremia and slower disease progression [79]. On the other hand, the activating allele KIR3DS1 has been associated with lower viremia and a delayed progression to AIDS when found alone [80] or in combination with HLA Bw4 molecules that have an isoleucine at position 80 (Bw4-80I) [81, 82]. Functionally, KIR3DS1 has been shown to correlate with strong inhibition of HIV-1 replication [83] and with higher NK cell effector functions in early HIV disease [84]. Recent studies also suggest that KIR3DL1 and KIR3DS1 could also play a role in differential susceptibility to HIV infection [85, 86].

c. Other immune-related molecules

All human genes that are related to immunity or inflammation can be suspected to play a role in HIV-1 pathogenesis. Many of them have been the subject of genetic studies: for example, polymorphisms in genes coding for several cytokines and cytokine receptors, which are key regulators of the inflammatory homeostasis, have been associated with both resistance to HIV-1 infection and progression of the disease. Yet, in the absence of conclusive replication, most of the associations published so far remain controversial.

Defensins are small peptides produced mainly by epithelial cells to help fight pathogens, including HIV-1. A variant located in the 5′ region of the β-defensin 1 gene (DEFB1) has been associated with higher level of HIV-1 RNA in breast milk [87]and with an increased risk of maternal-fetal transmission of the infection [88, 89].

The mannose-binding lectin 2 protein, encoded by the MBL2 gene, is an important element of the innate immune system that is capable of activating the classical complement pathway. MBL2-deficiencies have been associated with susceptibility to autoimmune and infectious diseases. Several non-synonymous coding variants have been associated with lower serum levels of MBL2, as well as increased susceptibility to HIV-1 infection and/or accelerated disease progression [90-92].

DC-SIGN, or CD209, is a gene encoding a trans-membrane C-type lectin with an extracellular portion composed of a tandem repeat region (“neck region”) and a carbohydrate recognition domain, which is important for pathogen binding. Neck region alleles with <5 repeat units were recently shown to associate with HVI-1 resistance in Chinese [93]. Conflicting results have also been reported regarding associations between DC-SIGN promoter polymorphisms and HIV-1 outcomes [94, 95]

Finally, recent evidence that HIV-1-derived products are able to activate an immune cells through Toll-like receptor (TLR) signaling lead to the description of genetic variants in TLR genes that associate with different rates of disease progression [96-98].

Conclusion

The mission of HIV host genetics is to describe as comprehensively as possible human genetic influences on HIV control. Even if a number of genetic factors implicated in HIV-1 pathogenesis have been described over the past 15 years, progress is arguably slow, mainly because of the number of studies with equivocal or controversial results. Technical limitations to genetic studies have now largely been overcome, but there are still too many flaws in HIV host genetic studies that could and should be addressed: clinical outcomes and biological phenotypes should be very precisely defined; the use of ancestry markers to correct for population stratification should now be the rule; large cohorts of ethnically diverse origin should be analyzed to decrease the likelihood of false positive findings and increase the coverage of human diversity. The goal is to provide the HIV research community with complete, powered and definitive studies on clear endpoints.

To make genetic studies easier to design and quicker to run, an critical step would be to include in the routine of all prospective cohorts a request for genetic consent, and also to obtain the permission to perform additional analyses as defined by local or national guidelines (e.g., waiver for deceased subjects or authorization to study cohorts under anonymity).

Genome-wide association studies have recently become the approach of choice to search for host factors involved in HIV-related outcomes and to assess their relative contribution [64-66]. They notably demonstrated the primary role of the MHC region in HIV-1 control. Still, these studies are only designed to detect common polymorphisms (generally >5% minor allele frequency) with effect sizes that are large enough to create significant associations after correction multiple testing. More common variants with smaller population effect sizes could be identified through a continuous increase in the number of subjects included in genome-wide studies. However, since rare genetic variants also play a role in the inter-individual variability of HIV phenotypes, targeted or whole-genome resequencing strategies will prove essential to better appreciate the global contribution of the human genome to HIV-1 control.

The ongoing historical transition into the genomic era brings new hopes that host genetics will contribute substantially to understanding HIV-1 pathogenesis. This will in turn help identify new targets for drug and vaccine development and potentially lead to the creation of predictive tools that would set the stage for personalized HIV medicine.

Acknowledgments

I am grateful to Amalio Telenti and David Goldstein for their advice and careful reading of the manuscript.

REFERENCES

1. O'Brien SJ, Nelson GW. Human genes that limit AIDS. Nat Genet. 2004;36:565–574. [PubMed]
2. Telenti A, Bleiber G. Host genetics of HIV-1 susceptibility. Future Virology. 2006;1:55–70.
3. Lama J, Planelles V. Host factors influencing susceptibility to HIV infection and AIDS progression. Retrovirology. 2007;4:52. [PMC free article] [PubMed]
4. Telenti A, Goldstein DB. Genomics meets HIV-1. Nat Rev Microbiol. 2006;4:865–873. [PMC free article] [PubMed]
5. Dean M, Carrington M, Winkler C, Huttley GA, Smith MW, Allikmets R, Goedert JJ, Buchbinder SP, Vittinghoff E, Gomperts E, Donfield S, Vlahov D, Kaslow R, Saah A, Rinaldo C, Detels R, O'Brien SJ. Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structural gene. Hemophilia Growth and Development Study, Multicenter AIDS Cohort Study, Multicenter Hemophilia Cohort Study, San Francisco City Cohort, ALIVE Study. Science. 1996;273:1856–1862. [PubMed]
6. Samson M, Libert F, Doranz BJ, Rucker J, Liesnard C, Farber CM, Saragosti S, Lapoumeroulie C, Cognaux J, Forceille C, Muyldermans G, Verhofstede C, Burtonboy G, Georges M, Imai T, Rana S, Yi Y, Smyth RJ, Collman RG, Doms RW, Vassart G, Parmentier M. Resistance to HIV-1 infection in caucasian individuals bearing mutant alleles of the CCR-5 chemokine receptor gene. Nature. 1996;382:722–725. [PubMed]
7. Liu R, Paxton WA, Choe S, Ceradini D, Martin SR, Horuk R, MacDonald ME, Stuhlmann H, Koup RA, Landau NR. Homozygous defect in HIV-1 coreceptor accounts for resistance of some multiply-exposed individuals to HIV-1 infection. Cell. 1996;86:367–377. [PubMed]
8. Huang Y, Paxton WA, Wolinsky SM, Neumann AU, Zhang L, He T, Kang S, Ceradini D, Jin Z, Yazdanbakhsh K, Kunstman K, Erickson D, Dragon E, Landau NR, Phair J, Ho DD, Koup RA. The role of a mutant CCR5 allele in HIV-1 transmission and disease progression. Nat Med. 1996;2:1240–1243. [PubMed]
9. Carrington M, Kissner T, Gerrard B, Ivanov S, O'Brien SJ, Dean M. Novel alleles of the chemokine-receptor gene CCR5. Am J Hum Genet. 1997;61:1261–1267. [PMC free article] [PubMed]
10. Ansari-Lari MA, Liu XM, Metzker ML, Rut AR, Gibbs RA. The extent of genetic variation in the CCR5 gene. Nat Genet. 1997;16:221–222. [PubMed]
11. Blanpain C, Lee B, Tackoen M, Puffer B, Boom A, Libert F, Sharron M, Wittamer V, Vassart G, Doms RW, Parmentier M. Multiple nonfunctional alleles of CCR5 are frequent in various human populations. Blood. 2000;96:1638–1645. [PubMed]
12. Capoulade-Metay C, Ma L, Truong LX, Dudoit Y, Versmisse P, Nguyen NV, Nguyen M, Scott-Algara D, Barre-Sinoussi F, Debre P, Bismuth G, Pancino G, Theodorou I. New CCR5 variants associated with reduced HIV coreceptor function in southeast Asia. Aids. 2004;18:2243–2252. [PubMed]
13. Quillent C, Oberlin E, Braun J, Rousset D, Gonzalez-Canali G, Metais P, Montagnier L, Virelizier JL, Arenzana-Seisdedos F, Beretta A. HIV-1-resistance phenotype conferred by combination of two separate inherited mutations of CCR5 gene. Lancet. 1998;351:14–18. [PubMed]
14. Wu L, Paxton WA, Kassam N, Ruffing N, Rottman JB, Sullivan N, Choe H, Sodroski J, Newman W, Koup RA, Mackay CR. CCR5 levels and expression pattern correlate with infectability by macrophage-tropic HIV-1, in vitro. J Exp Med. 1997;185:1681–1691. [PMC free article] [PubMed]
15. Martin MP, Dean M, Smith MW, Winkler C, Gerrard B, Michael NL, Lee B, Doms RW, Margolick J, Buchbinder S, Goedert JJ, O'Brien TR, Hilgartner MW, Vlahov D, O'Brien SJ, Carrington M. Genetic acceleration of AIDS progression by a promoter variant of CCR5. Science. 1998;282:1907–1911. [PubMed]
16. Mummidi S, Ahuja SS, Gonzalez E, Anderson SA, Santiago EN, Stephan KT, Craig FE, O'Connell P, Tryon V, Clark RA, Dolan MJ, Ahuja SK. Genealogy of the CCR5 locus and chemokine system gene variants associated with altered rates of HIV-1 disease progression. Nat Med. 1998;4:786–793. [PubMed]
17. Gonzalez E, Bamshad M, Sato N, Mummidi S, Dhanda R, Catano G, Cabrera S, McBride M, Cao XH, Merrill G, O'Connell P, Bowden DW, Freedman BI, Anderson SA, Walter EA, Evans JS, Stephan KT, Clark RA, Tyagi S, Ahuja SS, Dolan MJ, Ahuja SK. Race-specific HIV-1 disease-modifying effects associated with CCR5 haplotypes. Proc Natl Acad Sci U S A. 1999;96:12004–12009. [PMC free article] [PubMed]
18. Smith MW, Dean M, Carrington M, Winkler C, Huttley GA, Lomb DA, Goedert JJ, O'Brien TR, Jacobson LP, Kaslow R, Buchbinder S, Vittinghoff E, Vlahov D, Hoots K, Hilgartner MW, O'Brien SJ. Contrasting genetic influence of CCR2 and CCR5 variants on HIV-1 infection and disease progression. Hemophilia Growth and Development Study (HGDS), Multicenter AIDS Cohort Study (MACS), Multicenter Hemophilia Cohort Study (MHCS), San Francisco City Cohort (SFCC), ALIVE Study. Science. 1997;277:959–965. [PubMed]
19. Nakayama EE, Tanaka Y, Nagai Y, Iwamoto A, Shioda T. A CCR2-V64I polymorphism affects stability of CCR2A isoform. Aids. 2004;18:729–738. [PubMed]
20. Lee B, Doranz BJ, Rana S, Yi Y, Mellado M, Frade JM, Martinez AC, O'Brien SJ, Dean M, Collman RG, Doms RW. Influence of the CCR2-V64I polymorphism on human immunodeficiency virus type 1 coreceptor activity and on chemokine receptor function of CCR2b, CCR3, CCR5, and CXCR4. J Virol. 1998;72:7450–7458. [PMC free article] [PubMed]
21. Mariani R, Wong S, Mulder LC, Wilkinson DA, Reinhart AL, LaRosa G, Nibbs R, O'Brien TR, Michael NL, Connor RI, Macdonald M, Busch M, Koup RA, Landau NR. CCR2-64I polymorphism is not associated with altered CCR5 expression or coreceptor function. J Virol. 1999;73:2450–2459. [PMC free article] [PubMed]
22. Faure S, Meyer L, Costagliola D, Vaneensberghe C, Genin E, Autran B, Delfraissy JF, McDermott DH, Murphy PM, Debre P, Theodorou I, Combadiere C. Rapid progression to AIDS in HIV+ individuals with a structural variant of the chemokine receptor CX3CR1. Science. 2000;287:2274–2277. [PubMed]
23. Singh KK, Hughes MD, Chen J, Spector SA. Genetic polymorphisms in CX3CR1 predict HIV-1 disease progression in children independently of CD4+ lymphocyte count and HIV-1 RNA load. J Infect Dis. 2005;191:1971–1980. [PubMed]
24. Vidal F, Vilades C, Domingo P, Broch M, Pedrol E, Dalmau D, Knobel H, Peraire J, Gutierrez C, Sambeat MA, Fontanet A, Deig E, Cairo M, Montero M, Richart C, Mallal S. Spanish HIV-1-infected long-term nonprogressors of more than 15 years have an increased frequency of the CX3CR1 249I variant allele. J Acquir Immune Defic Syndr. 2005;40:527–531. [PubMed]
25. Duggal P, An P, Beaty TH, Strathdee SA, Farzadegan H, Markham RB, Johnson L, O'Brien SJ, Vlahov D, Winkler CA. Genetic influence of CXCR6 chemokine receptor alleles on PCP-mediated AIDS progression among African Americans. Genes Immun. 2003;4:245–250. [PubMed]
26. Vasilescu A, Terashima Y, Enomoto M, Heath S, Poonpiriya V, Gatanaga H, Do H, Diop G, Hirtzig T, Auewarakul P, Lauhakirti D, Sura T, Charneau P, Marullo S, Therwath A, Oka S, Kanegasaki S, Lathrop M, Matsushima K, Zagury JF, Matsuda F. A haplotype of the human CXCR1 gene protective against rapid disease progression in HIV-1+ patients. Proc Natl Acad Sci U S A. 2007;104:3354–3359. [PMC free article] [PubMed]
27. He W, Neil S, Kulkarni H, Wright E, Agan BK, Marconi VC, Dolan MJ, Weiss RA, Ahuja SK. Duffy antigen receptor for chemokines mediates trans-infection of HIV-1 from red blood cells to target cells and affects HIV-AIDS susceptibility. Cell Host Microbe. 2008;4:52–62. [PMC free article] [PubMed]
28. Paxton WA, Liu R, Kang S, Wu L, Gingeras TR, Landau NR, Mackay CR, Koup RA. Reduced HIV-1 infectability of CD4+ lymphocytes from exposed-uninfected individuals: association with low expression of CCR5 and high production of beta-chemokines. Virology. 1998;244:66–73. [PubMed]
29. Saha K, Bentsman G, Chess L, Volsky DJ. Endogenous production of beta-chemokines by CD4+, but not CD8+, T-cell clones correlates with the clinical state of human immunodeficiency virus type 1 (HIV-1)-infected individuals and may be responsible for blocking infection with non-syncytium-inducing HIV-1 in vitro. J Virol. 1998;72:876–881. [PMC free article] [PubMed]
30. McDermott DH, Beecroft MJ, Kleeberger CA, Al-Sharif FM, Ollier WE, Zimmerman PA, Boatin BA, Leitman SF, Detels R, Hajeer AH, Murphy PM. Chemokine RANTES promoter polymorphism affects risk of both HIV infection and disease progression in the Multicenter AIDS Cohort Study. Aids. 2000;14:2671–2678. [PubMed]
31. An P, Nelson GW, Wang L, Donfield S, Goedert JJ, Phair J, Vlahov D, Buchbinder S, Farrar WL, Modi W, O'Brien SJ, Winkler CA. Modulating influence on HIV/AIDS by interacting RANTES gene variants. Proc Natl Acad Sci U S A. 2002;99:10002–10007. [PMC free article] [PubMed]
32. Gonzalez E, Dhanda R, Bamshad M, Mummidi S, Geevarghese R, Catano G, Anderson SA, Walter EA, Stephan KT, Hammer MF, Mangano A, Sen L, Clark RA, Ahuja SS, Dolan MJ, Ahuja SK. Global survey of genetic variation in CCR5, RANTES, and MIP-1alpha: impact on the epidemiology of the HIV-1 pandemic. Proc Natl Acad Sci U S A. 2001;98:5199–5204. [PMC free article] [PubMed]
33. Liu H, Chao D, Nakayama EE, Taguchi H, Goto M, Xin X, Takamatsu JK, Saito H, Ishikawa Y, Akaza T, Juji T, Takebe Y, Ohishi T, Fukutake K, Maruyama Y, Yashiki S, Sonoda S, Nakamura T, Nagai Y, Iwamoto A, Shioda T. Polymorphism in RANTES chemokine promoter affects HIV-1 disease progression. Proc Natl Acad Sci U S A. 1999;96:4581–4585. [PMC free article] [PubMed]
34. Duggal P, Winkler CA, An P, Yu XF, Farzadegan H, O'Brien SJ, Beaty TH, Vlahov D. The effect of RANTES chemokine genetic variants on early HIV-1 plasma RNA among African American injection drug users. J Acquir Immune Defic Syndr. 2005;38:584–589. [PubMed]
35. Modi WS, Lautenberger J, An P, Scott K, Goedert JJ, Kirk GD, Buchbinder S, Phair J, Donfield S, O'Brien SJ, Winkler C. Genetic variation in the CCL18-CCL3-CCL4 chemokine gene cluster influences HIV Type 1 transmission and AIDS disease progression. Am J Hum Genet. 2006;79:120–128. [PMC free article] [PubMed]
36. Gonzalez E, Kulkarni H, Bolivar H, Mangano A, Sanchez R, Catano G, Nibbs RJ, Freedman BI, Quinones MP, Bamshad MJ, Murthy KK, Rovin BH, Bradley W, Clark RA, Anderson SA, O'Connell RJ, Agan BK, Ahuja SS, Bologna R, Sen L, Dolan MJ, Ahuja SK. The influence of CCL3L1 gene-containing segmental duplications on HIV-1/AIDS susceptibility. Science. 2005;307:1434–1440. [PubMed]
37. Dolan MJ, Kulkarni H, Camargo JF, He W, Smith A, Anaya JM, Miura T, Hecht FM, Mamtani M, Pereyra F, Marconi V, Mangano A, Sen L, Bologna R, Clark RA, Anderson SA, Delmar J, O'Connell RJ, Lloyd A, Martin J, Ahuja SS, Agan BK, Walker BD, Deeks SG, Ahuja SK. CCL3L1 and CCR5 influence cell-mediated immunity and affect HIV-AIDS pathogenesis via viral entry-independent mechanisms. Nat Immunol. 2007;8:1324–1336. [PubMed]
38. Modi WS, Goedert JJ, Strathdee S, Buchbinder S, Detels R, Donfield S, O'Brien SJ, Winkler C. MCP-1-MCP-3-Eotaxin gene cluster influences HIV-1 transmission. Aids. 2003;17:2357–2365. [PubMed]
39. Singh KK, Hughes MD, Chen J, Spector SA. Impact of MCP-1-2518-G allele on the HIV-1 disease of children in the United States. Aids. 2006;20:475–478. [PubMed]
40. Gonzalez E, Rovin BH, Sen L, Cooke G, Dhanda R, Mummidi S, Kulkarni H, Bamshad MJ, Telles V, Anderson SA, Walter EA, Stephan KT, Deucher M, Mangano A, Bologna R, Ahuja SS, Dolan MJ, Ahuja SK. HIV-1 infection and AIDS dementia are influenced by a mutant MCP-1 allele linked to increased monocyte infiltration of tissues and MCP-1 levels. Proc Natl Acad Sci U S A. 2002;99:13795–13800. [PMC free article] [PubMed]
41. Mummidi S, Bonello GB, Ahuja SK. Confirmation of differential binding of Interferon Regulatory Factor-1 (IRF-1) to the functional and HIV disease-influencing −2578 A/G polymorphism in CCL2. Genes Immun. 2008 [PubMed]
42. van Rij RP, Broersen S, Goudsmit J, Coutinho RA, Schuitemaker H. The role of a stromal cell-derived factor-1 chemokine gene variant in the clinical course of HIV-1 infection. Aids. 1998;12:F85–90. [PubMed]
43. Winkler C, Modi W, Smith MW, Nelson GW, Wu X, Carrington M, Dean M, Honjo T, Tashiro K, Yabe D, Buchbinder S, Vittinghoff E, Goedert JJ, O'Brien TR, Jacobson LP, Detels R, Donfield S, Willoughby A, Gomperts E, Vlahov D, Phair J, O'Brien SJ. Genetic restriction of AIDS pathogenesis by an SDF-1 chemokine gene variant. ALIVE Study, Hemophilia Growth and Development Study (HGDS), Multicenter AIDS Cohort Study (MACS), Multicenter Hemophilia Cohort Study (MHCS), San Francisco City Cohort (SFCC) Science. 1998;279:389–393. [PubMed]
44. Bleiber G, May M, Martinez R, Meylan P, Ott J, Beckmann JS, Telenti A. Use of a combined ex vivo/in vivo population approach for screening of human genes involved in the human immunodeficiency virus type 1 life cycle for variants influencing disease progression. J Virol. 2005;79:12674–12680. [PMC free article] [PubMed]
45. Magierowska M, Theodorou I, Debre P, Sanson F, Autran B, Riviere Y, Charron D, Costagliola D. Combined genotypes of CCR5, CCR2, SDF1, and HLA genes can predict the long-term nonprogressor status in human immunodeficiency virus-1-infected individuals. Blood. 1999;93:936–941. [PubMed]
46. Ioannidis JP, Rosenberg PS, Goedert JJ, Ashton LJ, Benfield TL, Buchbinder SP, Coutinho RA, Eugen-Olsen J, Gallart T, Katzenstein TL, Kostrikis LG, Kuipers H, Louie LG, Mallal SA, Margolick JB, Martinez OP, Meyer L, Michael NL, Operskalski E, Pantaleo G, Rizzardi GP, Schuitemaker H, Sheppard HW, Stewart GJ, Theodorou ID, Ullum H, Vicenzi E, Vlahov D, Wilkinson D, Workman C, Zagury JF, O'Brien TR. Effects of CCR5-Delta32, CCR2-64I, and SDF-1 3′A alleles on HIV-1 disease progression: An international meta-analysis of individual-patient data. Ann Intern Med. 2001;135:782–795. [PubMed]
47. Brass AL, Dykxhoorn DM, Benita Y, Yan N, Engelman A, Xavier RJ, Lieberman J, Elledge SJ. Identification of host proteins required for HIV infection through a functional genomic screen. Science. 2008;319:921–926. [PubMed]
48. Konig R, Zhou Y, Elleder D, Diamond TL, Bonamy GM, Irelan JT, Chiang CY, Tu BP, De Jesus PD, Lilley CE, Seidel S, Opaluch AM, Caldwell JS, Weitzman MD, Kuhen KL, Bandyopadhyay S, Ideker T, Orth AP, Miraglia LJ, Bushman FD, Young JA, Chanda SK. Global analysis of host-pathogen interactions that regulate early-stage HIV-1 replication. Cell. 2008;135:49–60. [PMC free article] [PubMed]
49. Zhou H, Xu M, Huang Q, Gates AT, Zhang XD, Castle JC, Stec E, Ferrer M, Strulovici B, Hazuda DJ, Espeseth AS. Genome-scale RNAi screen for host factors required for HIV replication. Cell Host Microbe. 2008;4:495–504. [PubMed]
50. Bashirova AA, Bleiber G, Qi Y, Hutcheson H, Yamashita T, Johnson RC, Cheng J, Alter G, Goedert JJ, Buchbinder S, Hoots K, Vlahov D, May M, Maldarelli F, Jacobson L, O'Brien SJ, Telenti A, Carrington M. Consistent effects of TSG101 genetic variability on multiple outcomes of exposure to human immunodeficiency virus type 1. J Virol. 2006;80:6757–6763. [PMC free article] [PubMed]
51. Bosco DA, Eisenmesser EZ, Pochapsky S, Sundquist WI, Kern D. Catalysis of cis/trans isomerization in native HIV-1 capsid by human cyclophilin A. Proc Natl Acad Sci U S A. 2002;99:5247–5252. [PMC free article] [PubMed]
52. Berthoux L, Sebastian S, Sokolskaja E, Luban J. Cyclophilin A is required for TRIM5{alpha}-mediated resistance to HIV-1 in Old World monkey cells. Proc Natl Acad Sci U S A. 2005;102:14849–14853. [PMC free article] [PubMed]
53. An P, Wang LH, Hutcheson-Dilks H, Nelson G, Donfield S, Goedert JJ, Rinaldo CR, Buchbinder S, Kirk GD, O'Brien SJ, Winkler CA. Regulatory polymorphisms in the cyclophilin A gene, PPIA, accelerate progression to AIDS. PLoS Pathog. 2007;3:e88. [PMC free article] [PubMed]
54. Rits MA, van Dort KA, Kootstra NA. Polymorphisms in the regulatory region of the Cyclophilin A gene influence the susceptibility for HIV-1 infection. PLoS ONE. 2008;3:e3975. [PMC free article] [PubMed]
55. Goldschmidt V, Bleiber G, May M, Martinez R, Ortiz M, Telenti A. Role of common human TRIM5alpha variants in HIV-1 disease progression. Retrovirology. 2006;3:54. [PMC free article] [PubMed]
56. Javanbakht H, An P, Gold B, Petersen DC, O'Huigin C, Nelson GW, O'Brien SJ, Kirk GD, Detels R, Buchbinder S, Donfield S, Shulenin S, Song B, Perron MJ, Stremlau M, Sodroski J, Dean M, Winkler C. Effects of human TRIM5alpha polymorphisms on antiretroviral function and susceptibility to human immunodeficiency virus infection. Virology. 2006;354:15–27. [PubMed]
57. Nakayama EE, Carpentier W, Costagliola D, Shioda T, Iwamoto A, Debre P, Yoshimura K, Autran B, Matsushita S, Theodorou I. Wild type and H43Y variant of human TRIM5alpha show similar anti-human immunodeficiency virus type 1 activity both in vivo and in vitro. Immunogenetics. 2007;59:511–515. [PubMed]
58. van Manen D, Rits MA, Beugeling C, van Dort K, Schuitemaker H, Kootstra NA. The effect of Trim5 polymorphisms on the clinical course of HIV-1 infection. PLoS Pathog. 2008;4:e18. [PMC free article] [PubMed]
59. Sheehy AM, Gaddis NC, Choi JD, Malim MH. Isolation of a human gene that inhibits HIV-1 infection and is suppressed by the viral Vif protein. Nature. 2002;418:646–650. [PubMed]
60. An P, Bleiber G, Duggal P, Nelson G, May M, Mangeat B, Alobwede I, Trono D, Vlahov D, Donfield S, Goedert JJ, Phair J, Buchbinder S, O'Brien SJ, Telenti A, Winkler CA. APOBEC3G genetic variants and their influence on the progression to AIDS. J Virol. 2004;78:11070–11076. [PMC free article] [PubMed]
61. Do H, Vasilescu A, Diop G, Hirtzig T, Heath SC, Coulonges C, Rappaport J, Therwath A, Lathrop M, Matsuda F, Zagury JF. Exhaustive genotyping of the CEM15 (APOBEC3G) gene and absence of association with AIDS progression in a French cohort. J Infect Dis. 2005;191:159–163. [PubMed]
62. Migueles SA, Sabbaghian MS, Shupert WL, Bettinotti MP, Marincola FM, Martino L, Hallahan CW, Selig SM, Schwartz D, Sullivan J, Connors M. HLA B*5701 is highly associated with restriction of virus replication in a subgroup of HIV-infected long term nonprogressors. Proc Natl Acad Sci U S A. 2000;97:2709–2714. [PMC free article] [PubMed]
63. Altfeld M, Addo MM, Rosenberg ES, Hecht FM, Lee PK, Vogel M, Yu XG, Draenert R, Johnston MN, Strick D, Allen TM, Feeney ME, Kahn JO, Sekaly RP, Levy JA, Rockstroh JK, Goulder PJ, Walker BD. Influence of HLA-B57 on clinical presentation and viral control during acute HIV-1 infection. Aids. 2003;17:2581–2591. [PubMed]
64. Fellay J, Shianna KV, Ge D, Colombo S, Ledergerber B, Weale M, Zhang K, Gumbs C, Castagna A, Cossarizza A, Cozzi-Lepri A, De Luca A, Easterbrook P, Francioli P, Mallal S, Martinez-Picado J, Miro JM, Obel N, Smith JP, Wyniger J, Descombes P, Antonarakis SE, Letvin NL, McMichael AJ, Haynes BF, Telenti A, Goldstein DB. A whole-genome association study of major determinants for host control of HIV-1. Science. 2007;317:944–947. [PMC free article] [PubMed]
65. Limou S, Le Clerc S, Coulonges C, Carpentier W, Dina C, Delaneau O, Labib T, Taing L, Sladek R, Deveau C, Ratsimandresy R, Montes M, Spadoni JL, Lelievre JD, Levy Y, Therwath A, Schachter F, Matsuda F, Gut I, Froguel P, Delfraissy JF, Hercberg S, Zagury JF. Genomewide Association Study of an AIDS-Nonprogression Cohort Emphasizes the Role Played by HLA Genes (ANRS Genomewide Association Study 02) J Infect Dis. 2008 [PubMed]
66. Dalmasso C, Carpentier W, Meyer L, Rouzioux C, Goujard C, Chaix ML, Lambotte O, Avettand-Fenoel V, Le Clerc S, de Senneville LD, Deveau C, Boufassa F, Debre P, Delfraissy JF, Broet P, Theodorou I. Distinct genetic loci control plasma HIV-RNA and cellular HIV-DNA levels in HIV-1 infection: the ANRS Genome Wide Association 01 study. PLoS ONE. 2008;3:e3907. [PMC free article] [PubMed]
67. Goulder PJ, Phillips RE, Colbert RA, McAdam S, Ogg G, Nowak MA, Giangrande P, Luzzi G, Morgan B, Edwards A, McMichael AJ, Rowland-Jones S. Late escape from an immunodominant cytotoxic T-lymphocyte response associated with progression to AIDS. Nat Med. 1997;3:212–217. [PubMed]
68. Schneidewind A, Brockman MA, Yang R, Adam RI, Li B, Le Gall S, Rinaldo CR, Craggs SL, Allgaier RL, Power KA, Kuntzen T, Tung CS, LaBute MX, Mueller SM, Harrer T, McMichael AJ, Goulder PJ, Aiken C, Brander C, Kelleher AD, Allen TM. Escape from the dominant HLA-B27-restricted cytotoxic T-lymphocyte response in Gag is associated with a dramatic reduction in human immunodeficiency virus type 1 replication. J Virol. 2007;81:12382–12393. [PMC free article] [PubMed]
69. Gao X, Nelson GW, Karacki P, Martin MP, Phair J, Kaslow R, Goedert JJ, Buchbinder S, Hoots K, Vlahov D, O'Brien SJ, Carrington M. Effect of a single amino acid change in MHC class I molecules on the rate of progression to AIDS. N Engl J Med. 2001;344:1668–1675. [PubMed]
70. Carrington M, Nelson GW, Martin MP, Kissner T, Vlahov D, Goedert JJ, Kaslow R, Buchbinder S, Hoots K, O'Brien SJ. HLA and HIV-1: heterozygote advantage and B*35-Cw*04 disadvantage. Science. 1999;283:1748–1752. [PubMed]
71. Steel CM, Ludlam CA, Beatson D, Peutherer JF, Cuthbert RJ, Simmonds P, Morrison H, Jones M. HLA haplotype A1 B8 DR3 as a risk factor for HIV-related disease. Lancet. 1988;1:1185–1188. [PubMed]
72. Trachtenberg E, Korber B, Sollars C, Kepler TB, Hraber PT, Hayes E, Funkhouser R, Fugate M, Theiler J, Hsu YS, Kunstman K, Wu S, Phair J, Erlich H, Wolinsky S. Advantage of rare HLA supertype in HIV disease progression. Nat Med. 2003;9:928–935. [PubMed]
73. Dorak MT, Tang J, Tang S, Penman-Aguilar A, Coutinho RA, Goedert JJ, Detels R, Kaslow RA. Influence of human leukocyte antigen-B22 alleles on the course of human immunodeficiency virus type 1 infection in 3 cohorts of white men. J Infect Dis. 2003;188:856–863. [PubMed]
74. Kaslow RA, Carrington M, Apple R, Park L, Munoz A, Saah AJ, Goedert JJ, Winkler C, O'Brien SJ, Rinaldo C, Detels R, Blattner W, Phair J, Erlich H, Mann DL. Influence of combinations of human major histocompatibility complex genes on the course of HIV-1 infection. Nat Med. 1996;2:405–411. [PubMed]
75. Flores-Villanueva PO, Hendel H, Caillat-Zucman S, Rappaport J, Burgos-Tiburcio A, Bertin-Maghit S, Ruiz-Morales JA, Teran ME, Rodriguez-Tafur J, Zagury JF. Associations of MHC ancestral haplotypes with resistance/susceptibility to AIDS disease development. J Immunol. 2003;170:1925–1929. [PubMed]
76. Tang J, Costello C, Keet IP, Rivers C, Leblanc S, Karita E, Allen S, Kaslow RA. HLA class I homozygosity accelerates disease progression in human immunodeficiency virus type 1 infection. AIDS Res Hum Retroviruses. 1999;15:317–324. [PubMed]
77. Goulder PJ, Bunce M, Luzzi G, Phillips RE, McMichael AJ. Potential underestimation of HLA-C-restricted cytotoxic T-lymphocyte responses. Aids. 1997;11:1884–1886. [PubMed]
78. Carrington M, Martin MP, van Bergen J. KIR-HLA intercourse in HIV disease. Trends Microbiol. 2008;16:620–627. [PMC free article] [PubMed]
79. Martin MP, Qi Y, Gao X, Yamada E, Martin JN, Pereyra F, Colombo S, Brown EE, Shupert WL, Phair J, Goedert JJ, Buchbinder S, Kirk GD, Telenti A, Connors M, O'Brien SJ, Walker BD, Parham P, Deeks SG, McVicar DW, Carrington M. Innate partnership of HLA-B and KIR3DL1 subtypes against HIV-1. Nat Genet. 2007;39:733–740. [PubMed]
80. Barbour JD, Sriram U, Caillier SJ, Levy JA, Hecht FM, Oksenberg JR. Synergy or independence? Deciphering the interaction of HLA Class I and NK cell KIR alleles in early HIV-1 disease progression. PLoS Pathog. 2007;3:e43. [PMC free article] [PubMed]
81. Martin MP, Gao X, Lee JH, Nelson GW, Detels R, Goedert JJ, Buchbinder S, Hoots K, Vlahov D, Trowsdale J, Wilson M, O'Brien SJ, Carrington M. Epistatic interaction between KIR3DS1 and HLA-B delays the progression to AIDS. Nat Genet. 2002;31:429–434. [PubMed]
82. Qi Y, Martin MP, Gao X, Jacobson L, Goedert JJ, Buchbinder S, Kirk GD, O'Brien SJ, Trowsdale J, Carrington M. KIR/HLA pleiotropism: protection against both HIV and opportunistic infections. PLoS Pathog. 2006;2:e79. [PMC free article] [PubMed]
83. Alter G, Martin MP, Teigen N, Carr WH, Suscovich TJ, Schneidewind A, Streeck H, Waring M, Meier A, Brander C, Lifson JD, Allen TM, Carrington M, Altfeld M. Differential natural killer cell-mediated inhibition of HIV-1 replication based on distinct KIR/HLA subtypes. J Exp Med. 2007;204:3027–3036. [PMC free article] [PubMed]
84. Long BR, Ndhlovu LC, Oksenberg JR, Lanier LL, Hecht FM, Nixon DF, Barbour JD. Conferral of enhanced natural killer cell function by KIR3DS1 in early human immunodeficiency virus type 1 infection. J Virol. 2008;82:4785–4792. [PMC free article] [PubMed]
85. Boulet S, Kleyman M, Kim JY, Kamya P, Sharafi S, Simic N, Bruneau J, Routy JP, Tsoukas CM, Bernard NF. A combined genotype of KIR3DL1 high expressing alleles and HLA-B*57 is associated with a reduced risk of HIV infection. Aids. 2008;22:1487–1491. [PubMed]
86. Boulet S, Sharafi S, Simic N, Bruneau J, Routy JP, Tsoukas CM, Bernard NF. Increased proportion of KIR3DS1 homozygotes in HIV-exposed uninfected individuals. Aids. 2008;22:595–599. [PubMed]
87. Baroncelli S, Ricci E, Andreotti M, Guidotti G, Germano P, Marazzi MC, Vella S, Palombi L, De Rossi A, Giuliano M. Single-nucleotide polymorphisms in human beta-defensin-1 gene in Mozambican HIV-1-infected women and correlation with virologic parameters. Aids. 2008;22:1515–1517. [PubMed]
88. Braida L, Boniotto M, Pontillo A, Tovo PA, Amoroso A, Crovella S. A single-nucleotide polymorphism in the human beta-defensin 1 gene is associated with HIV-1 infection in Italian children. Aids. 2004;18:1598–1600. [PubMed]
89. Milanese M, Segat L, Pontillo A, Arraes LC, de Lima Filho JL, Crovella S. DEFB1 gene polymorphisms and increased risk of HIV-1 infection in Brazilian children. Aids. 2006;20:1673–1675. [PubMed]
90. Garred P, Madsen HO, Balslev U, Hofmann B, Pedersen C, Gerstoft J, Svejgaard A. Susceptibility to HIV infection and progression of AIDS in relation to variant alleles of mannose-binding lectin. Lancet. 1997;349:236–240. [PubMed]
91. Boniotto M, Braida L, Pirulli D, Arraes L, Amoroso A, Crovella S. MBL2 polymorphisms are involved in HIV-1 infection in Brazilian perinatally infected children. Aids. 2003;17:779–780. [PubMed]
92. Vallinoto AC, Menezes-Costa MR, Alves AE, Machado LF, de Azevedo VN, Souza LL, Ishak Mde O, Ishak R. Mannose-binding lectin gene polymorphism and its impact on human immunodeficiency virus 1 infection. Mol Immunol. 2006;43:1358–1362. [PubMed]
93. Zhang J, Zhang X, Fu J, Bi Z, Arheart KL, Barreiro LB, Quintana-Murci L, Pahwa S, Liu H. Protective role of DC-SIGN (CD209) neck-region alleles with <5 repeat units in HIV-1 transmission. J Infect Dis. 2008;198:68–71. [PubMed]
94. Koizumi Y, Kageyama S, Fujiyama Y, Miyashita M, Lwembe R, Ogino K, Shioda T, Ichimura H. RANTES −28G delays and DC-SIGN - 139C enhances AIDS progression in HIV type 1-infected Japanese hemophiliacs. AIDS Res Hum Retroviruses. 2007;23:713–719. [PubMed]
95. Wichukchinda N, Kitamura Y, Rojanawiwat A, Nakayama EE, Song H, Pathipvanich P, Auwanit W, Sawanpanyalert P, Iwamoto A, Shioda T, Ariyoshi K. The polymorphisms in DC-SIGNR affect susceptibility to HIV type 1 infection. AIDS Res Hum Retroviruses. 2007;23:686–692. [PubMed]
96. Bochud PY, Hersberger M, Taffe P, Bochud M, Stein CM, Rodrigues SD, Calandra T, Francioli P, Telenti A, Speck RF, Aderem A. Polymorphisms in Toll-like receptor 9 influence the clinical course of HIV-1 infection. Aids. 2007;21:441–446. [PubMed]
97. Oh DY, Baumann K, Hamouda O, Eckert JK, Neumann K, Kucherer C, Bartmeyer B, Poggensee G, Oh N, Pruss A, Jessen H, Schumann RR. A frequent functional toll-like receptor 7 polymorphism is associated with accelerated HIV-1 disease progression. Aids. 2008 [PubMed]
98. Soriano-Sarabia N, Vallejo A, Ramirez-Lorca R, Rodriguez Mdel M, Salinas A, Pulido I, Saez ME, Leal M. Influence of the Toll-like receptor 9 1635A/G polymorphism on the CD4 count, HIV viral load, and clinical progression. J Acquir Immune Defic Syndr. 2008;49:128–135. [PubMed]
PubReader format: click here to try

Formats:

Related citations in PubMed

See reviews...See all...

Cited by other articles in PMC

See all...

Links

Recent Activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...