Human immunodeficiency virus type-2 (HIV-2) is a close relative of the prototype acquired immunodeficiency syndrome (AIDS) virus, HIV-1. HIV-2 is biologically similar to HIV-1, but information is lacking concerning clinical outcomes of HIV-2-infected individuals. From 1985 to 1993, a prospective clinical study was conducted in women with HIV-2 and HIV-1 infection to determine and compare rates of disease development. HIV-1-infected women had a 67% probability of AIDS-free survival 5 years after seroconversion in contrast with 100% for HIV-2-infected women. In addition to having significantly less HIV-related disease outcome in HIV-2 enrollees compared to HIV-1 enrollees, the rate of developing abnormal CD4+ lymphocyte counts with HIV-2 infection was also significantly reduced. This natural history study demonstrates that HIV-2 has a reduced virulence compared to HIV-1.

At least 10 different genetic human immunodeficiency virus type 1 (HIV-1) subtypes (A-J) are responsible for the AIDS pandemic. Much of the understanding of HIV-1 disease progression derives from studies in the developed world where HIV infection is almost exclusively subtype B. This has led many to question whether the properties and consequences of HIV-1 infection can be generalized across subtypes that afflict the majority of infected persons in the developing world. From 1985 to 1997, a prospective study of registered female sex workers in Senegal tracked the introduction and spread of HIV-1 subtypes A, C, D, and G. In clinical follow-up, the AIDS-free survival curves differed by HIV-1 subtype. Women infected with a non-A subtype were 8 times more likely to develop AIDS than were those infected with subtype A (hazard ratio=8.23; P=. 009), the predominant subtype in the study. These data suggest that HIV-1 subtypes may differ in rates of progression to AIDS.

With increasing survival of HIV-infected children, parents face the challenges of disclosure to the children. The aim of this study was to assess the rate of HIV disclosure to children in Ibadan and the factors influencing it in order to guide design of strategies for successful disclosure. A semi-structured questionnaire was administered to consecutive consenting caregivers of HIV-infected children aged ≥6 years attending the Paediatric Infectious Disease Clinic of the University College Hospital, Ibadan, between November 2008 and October 2009. Caregivers of 96 children (46 boys, 50 girls) infected with HIV were interviewed. The ages of the children ranged from 6 to 14 years with a mean (SD) of 8.8 (2.2) years. Disclosure had been done in only 13 (13.5%) of the children; ages at disclosure ranged from 4.5 to 13 years with a mean of 8.7 (SD = 2.2). Disclosure was associated with age above 10 years. Reasons given by carers for non-disclosure in 83 caregivers included inability of the children to understand in 53 (63.9%), fear of disclosure to other children 34 (41.0%), fear of disclosure to family/friends in 28 (33.7%), fear of psychological disturbance of the children in 26 (31.3%) and fear of blaming the parents in 22 (26.5%). Twenty (20.8%) of the children have asked questions relating to their diagnosis and the responses are often evasive. Caregivers felt disclosure had helped adherence to antiretroviral therapy in 7 (63.6%) of the 11 children on antiretroviral drugs in whom there was disclosure but no effect on the remaining. There is a need to assist parents and health care providers in successfully disclosing HIV status to infected children without adverse consequences.

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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 all samples tested; the median load was 141 copies/mL. Levels of viral RNA in the plasma were inversely related to CD4+ cell counts. HIV-2 and HIV-1 viral loads were compared among the seroincident women in the cohort; the median viral load was 30x lower in the HIV-2-infected women (P<.001, Wilcoxon rank sum test), irrespective of the length of time infected. This suggests that plasma viremia is linked to the differences in the pathogenicity of the 2 viruses.

SummaryBackgroundAntiretroviral therapy (ART) is crucial for controlling HIV-1 infection through wide-scale treatment as prevention and pre-exposure prophylaxis (PrEP). Potent tenofovir disoproxil fumarate-containing regimens are increasingly used to treat and prevent HIV, although few data exist for frequency and risk factors of acquired drug resistance in regions hardest hit by the HIV pandemic. We aimed to do a global assessment of drug resistance after virological failure with first-line tenofovir-containing ART.MethodsThe TenoRes collaboration comprises adult HIV treatment cohorts and clinical trials of HIV drug resistance testing in Europe, Latin and North America, sub-Saharan Africa, and Asia. We extracted and harmonised data for patients undergoing genotypic resistance testing after virological failure with a first-line regimen containing tenofovir plus a cytosine analogue (lamivudine or emtricitabine) plus a non-nucleotide reverse-transcriptase inhibitor (NNRTI; efavirenz or nevirapine). We used an individual participant-level meta-analysis and multiple logistic regression to identify covariates associated with drug resistance. Our primary outcome was tenofovir resistance, defined as presence of K65R/N or K70E/G/Q mutations in the reverse transcriptase (RT) gene.FindingsWe included 1926 patients from 36 countries with treatment failure between 1998 and 2015. Prevalence of tenofovir resistance was highest in sub-Saharan Africa (370/654 [57%]). Pre-ART CD4 cell count was the covariate most strongly associated with the development of tenofovir resistance (odds ratio [OR] 1·50, 95% CI 1·27–1·77 for CD4 cell count <100 cells per μL). Use of lamivudine versus emtricitabine increased the risk of tenofovir resistance across regions (OR 1·48, 95% CI 1·20–1·82). Of 700 individuals with tenofovir resistance, 578 (83%) had cytosine analogue resistance (M184V/I mutation), 543 (78%) had major NNRTI resistance, and 457 (65%) had both. The mean plasma viral load at virological failure was similar in individuals with and without tenofovir resistance (145 700 copies per mL [SE 12 480] versus 133 900 copies per mL [SE 16 650; p=0·626]).InterpretationWe recorded drug resistance in a high proportion of patients after virological failure on a tenofovir-containing first-line regimen across low-income and middle-income regions. Effective surveillance for transmission of drug resistance is crucial.FundingThe Wellcome Trust.

Background As HAART is introduced into areas of the world with high hepatitis B virus (HBV) endemicity, it is important to determine the influence of HBV on HIV-HBV co-infected persons receiving antiretroviral therapy (ART). Methods We studied 1,564 HIV-infected subjects in Jos, Nigeria who initiated ART. HIV-HBV co-infected participants had HBeAg and HBV DNA status determined. CD4+ T-cell count and HIV viral load at ART initiation were compared between HIV mono-infected and HIV-HBV co-infected subjects using univariate methods. Regression analyses were used to determine if HBeAg status or HBV DNA at ART initiation were associated with baseline HIV parameters or ART response. Results The CD4+ T-cell counts of the 262 (16.7%) HIV-HBV co-infected participants was 107 cells/mL compared to 130 cells/mL in HIV monoinfected participants (p <0.001) at ART initiation. HIV-HBV co-infected participants also had higher HIV viral loads than HIV monoinfected subjects (4.96 vs. 4.75 log10 copies/mL; p = 0.02). Higher HBV DNA and detectable HBeAg were independently associated with lower CD4+ T-cell counts at ART initiation but not with higher HIV viral load. In a multivariable model, HBeAg-positive subjects were less likely to suppress HIV replication to ≤400 copies/ml (OR 0.54, p=0.03) at 24 weeks, but they had similar CD4+ T cell increases. At 48 weeks, there was no significant effect of HBeAg status on ART response. Conclusions In HIV-infected Nigerian individuals, HBV co-infection, especially in those with high levels of HBV replication, was associated with lower CD4+ T-cell counts at ART initiation independent of HIV RNA level. Subjects with HBeAg positive status had a slower virological response to ART. Further work is needed to understand the effects of HBV on CD4+ T-cells.

A newly identified protein from HTLV-III/LAV, the virus implicated as the etiologic agent of the acquired immune deficiency syndrome, was studied. This protein, which has a molecular weight of 27,000 (p27), was shown by amino acid sequencing to have a coding origin 3' to the env gene on the HTLV-III genome. The presence of antibodies to p27 in virus-exposed individuals indicated that this gene is functional in the natural host.