Abstract:Human immunodeficiency virus type 2 (HIV-2) is less pathogenic than HIV type 1 (HIV-1), but the mechanisms underlying this difference have not been defined. We developed an internally controlled quantitative reverse transcriptase-polymerase chain reaction to measure HIV-2 viral load and determined levels of plasma virus in a cohort of registered commercial sex workers in Dakar, Senegal. The assay has a lower limit of detection of 100 copies/mL and is linear over 4 logs. HIV-2 viral RNA was detectable in 56% of… Show more
“…Most HIV-2 + individuals are long-term nonprogressors (LTNP) with low or undetectable viral loads [1,2]. Therefore, HIV-2 infection has the features of an 'attenuated' HIV-1 infection, but evidence for a true attenuated phenotype is lacking [3].…”
The mechanisms underlying the relatively slow progression of human immunodeficiency virus type 2 (HIV‐2) compared with HIV‐1 infection are undefined and could be a result of more effective immune responses. We used HIV‐2 and HIV‐1 IFN‐γ enzyme‐linked immunospot assays to evaluate CD8+ T cell responses in antiretroviral‐naive HIV‐2‐ (‘HIV‐2+’) and HIV‐1‐infected (‘HIV‐1+’) individuals. Gag‐specific responses were detected in the majority of HIV‐2+ and HIV‐1+ subjects. Overlapping gag peptide analysis indicated a significantly greater magnitude and breadth of responses in the HIV‐1+ cohort, and this difference was attributable to low responses in HIV‐2+ subjects with undetectable viral load (medians 2107 and 512 spot‐forming units per 106 PBMC, respectively, p=0.007). We investigated the phenotype of viral epitope‐specific CD8+ T cells identified with HLA‐B53‐ and HLA‐B58‐peptide tetramers (8 HIV‐2+, 11 HIV‐1+ subjects). HIV‐2‐specific CD8+ T cells were predominantly CD27+ CD45RA–, and only a minority expressed perforin. The limited breadth and low frequency of CD8+ T cell responses to HIV‐2 gag in aviremic HIV‐2+ subjects suggests that these responses reflect antigen load in plasma, as is the case in HIV‐1 infection. Immune control of HIV‐2 does not appear to be related to the frequency of perforin‐expressing virus‐specific CD8+ T cells.
“…Most HIV-2 + individuals are long-term nonprogressors (LTNP) with low or undetectable viral loads [1,2]. Therefore, HIV-2 infection has the features of an 'attenuated' HIV-1 infection, but evidence for a true attenuated phenotype is lacking [3].…”
The mechanisms underlying the relatively slow progression of human immunodeficiency virus type 2 (HIV‐2) compared with HIV‐1 infection are undefined and could be a result of more effective immune responses. We used HIV‐2 and HIV‐1 IFN‐γ enzyme‐linked immunospot assays to evaluate CD8+ T cell responses in antiretroviral‐naive HIV‐2‐ (‘HIV‐2+’) and HIV‐1‐infected (‘HIV‐1+’) individuals. Gag‐specific responses were detected in the majority of HIV‐2+ and HIV‐1+ subjects. Overlapping gag peptide analysis indicated a significantly greater magnitude and breadth of responses in the HIV‐1+ cohort, and this difference was attributable to low responses in HIV‐2+ subjects with undetectable viral load (medians 2107 and 512 spot‐forming units per 106 PBMC, respectively, p=0.007). We investigated the phenotype of viral epitope‐specific CD8+ T cells identified with HLA‐B53‐ and HLA‐B58‐peptide tetramers (8 HIV‐2+, 11 HIV‐1+ subjects). HIV‐2‐specific CD8+ T cells were predominantly CD27+ CD45RA–, and only a minority expressed perforin. The limited breadth and low frequency of CD8+ T cell responses to HIV‐2 gag in aviremic HIV‐2+ subjects suggests that these responses reflect antigen load in plasma, as is the case in HIV‐1 infection. Immune control of HIV‐2 does not appear to be related to the frequency of perforin‐expressing virus‐specific CD8+ T cells.
“…Whereas HIV-1 group M subtypes (A-D, F, H, J, and K) are spread globally, HIV-2 subtypes are mainly restricted to West Africa and can be categorized as epidemic subtypes (A and B) and nonepidemic subtypes (C-G) (4)(5)(6)(7). Biological reasons have been invoked to explain the difference in global epidemiology between HIV-1 and HIV-2, such as lower HIV-2 viral loads that correlate with a lower transmissibility (8)(9)(10). However, attempts to compare the history of the epidemics at their respective geographic origins are still lacking.…”
In this study we date the introduction of HIV-2 into the human population and estimate the epidemic history of HIV-2 subtype A in Guinea-Bissau, the putative geographic origin of HIV-2. The evolutionary history of the simian immunodeficiency virus sooty mangabey͞HIV-2 lineage was reconstructed by using available database sequences with known sampling dates, and a timescale for this history was calculated by using maximum likelihood methods. The date of the most recent common ancestor of HIV-2 subtype A strains was estimated to be 1940 ؎ 16 and that of B strains was estimated to be 1945 ؎ 14. In addition we used coalescent theory to estimate the past population dynamics of HIV-2 subtype A in a rural population of Guinea-Bissau. Parametric and nonparametric estimates of the effective number of infections through time were obtained for an equal sample of gag, pol, and env sequences. Our estimates of the epidemic history of HIV-2 subtype A in Guinea-Bissau show a transition from constant size to rapid exponential growth around 1955-1970. Our analysis provides evidence for a zoonotic transfer of HIV-2 during the first half of the 20th century and an epidemic initiation in Guinea-Bissau that coincides with the independence war (1963)(1964)(1965)(1966)(1967)(1968)(1969)(1970)(1971)(1972)(1973)(1974), suggesting that war-related changes in sociocultural patterns had a major impact on the HIV-2 epidemic.T he AIDS epidemic is clearly recognized as a viral zoonosis (1-3). Phylogenetic analysis indicates that multiple interspecies transmissions from simian species have introduced two genetically distinct types of HIV into the human population: HIV-1, closely related to simian immunodeficiency virus (SIV) from chimpanzees (SIV CPZ ), and HIV-2, closely related to SIV from sooty mangabeys (SIV SM ). Whereas HIV-1 group M subtypes (A-D, F, H, J, and K) are spread globally, HIV-2 subtypes are mainly restricted to West Africa and can be categorized as epidemic subtypes (A and B) and nonepidemic subtypes (C-G) (4-7). Biological reasons have been invoked to explain the difference in global epidemiology between HIV-1 and HIV-2, such as lower HIV-2 viral loads that correlate with a lower transmissibility (8-10). However, attempts to compare the history of the epidemics at their respective geographic origins are still lacking.A useful strategy for investigating the epidemic history of HIV combines molecular clock analysis, to estimate the timescale of the epidemic, and coalescent theory, to infer the demographic history of the virus (11). Various molecular clock calculations have dated the most recent common ancestor (MRCA) of HIV-1 group M around 1930 Ϯ 15 (12-14). HIV-1 group M has subsequently spread globally, generating the pandemic observed today. Here, we investigate the epidemic history of HIV-2 to test previously suggested hypotheses of its origin. We provide the first estimated dates of cross-species transmissions of HIV-2. Our results indicate a transfer of HIV-2 subtypes A and B from sooty mangabeys to humans during the fi...
“…Again, it might mean that this particular VBD was positive for HIV-2 which is less virulent and have lower progression to AIDS compared to HIV-1 [12]. Studies have showed the inverse relationships between HIV viral loads and CD4+ T-lymphocytes [45,46]. DOR adopted in this study validated the reliability of the results of rapid antibody techniques (based on serial algorithm II).…”
Background: The challenge of 'safe blood' practice has given rise to several unanswered questions in the practice of immune-hematology and has led to controversies as to which algorithm adopted for HIV testing in prospective blood donors pose the least risk and provide safe blood to recipients of blood transfusion. The aim of this study is to evaluate HIV epidemiology and the outcomes of CDC-UMD serial algorithm II for HIV antibody testing in our resource-limited setting by advancing HIV screening beyond serologic procedure.
Material and Methods:A total of 140 prospective blood donors were enrolled in the study between November, 2014 and July, 2015 by consecutive sampling technique. Study used HIV antibody screening based on serial algorithm II as the first-line testing protocol followed by ELISA technique. HIV-DNA confirmation and HIV-RNA quantification were carried out on pooled DBS and plasma samples respectively using real-time PCR.
Results:The overall mean age and gender ratio of PBD were 27.9±7.9 years and 1.1:1. Chi square analysis revealed that the PBD had the right knowledge of all the routes of HIV transmission (χ2 range: 63.3 -212.7, p< 0.05). Study showed an overall HIV prevalence of 2.9% irrespective of assay technique with intercategory variation in prevalence. Pooled sero-negative DBS samples analysis by real-time PCR showed absence of occult HIV infection among PBD and viral load of confirmed positive blood donors revealed low viraemia (least being 25copies/ mL).
Conclusion:Based on the study findings, HIV rapid antibody testing based on serial algorithm II did not compromise 'safe blood practice'. Adoption of rapid HIV antibody techniques based on serial algorithm II can serve as a surrogate HIV confirmatory technique in PBD where facilities for ELISA or the more costly realtime PCR are unavailable.
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