High magnitude of under nutrition among HIV infected adults who have not started ART in Tanzania--a call to include nutrition care and treatment in the test and treat model.

BACKGROUND: Undernutrition among people living with HIV (PLWHIV) can be ameliorated if nutrition specific and sensitive interventions are integrated into their HIV care and treatment centers (CTC). Integrated care is lacking despite expansion of antiretroviral therapy (ART) coverage, representing a substantial missed opportunity. This research aims to examine nutritional status and associated risk factors among HIV-positive adults prior to ART initiation in Tanzania in order to characterize existing gaps and inform early integration of nutrition care into CTC. METHODS: We analyzed data from 3993 pre-ART adults living with HIV enrolled in CTCs within the Trial of Vitamin (TOV3) and progression of HIV/AIDS study in Dar es salaam, Tanzania. The primary outcome for this analysis was undernutrition, measured as body mass index (BMI) below 18.5 kg/m2. We conducted descriptive analyses of baseline characteristics and utilized multiple logistic regression to determine independent factors associated with pre-ART undernutrition. RESULTS: Undernutrition was prevalent in about 27.7% of pre-ART adults, with a significantly higher magnitude among males compared to females (30% vs. 26.6%, p < 0.025). Severe undernutrition (BMI < 16.0 kg/m2) was prevalent in one in four persons, with a trend toward higher magnitudes among females (26.2% vs. 21.1% p = 0.123). Undernutrition was also more prevalent among younger adults (p < 0.001), those with lower wealth quintiles (p = 0.003), and those with advanced HIV clinical stage (p < 0.001). Pre-ART adults presented with poor feeding practices, hallmarked by low dietary diversity scores and infrequent consumption of proteins, vegetables, and fruits. After adjusting for confounders and important co-variates, pre-ART undernutrition was associated with younger age, low wealth indices, advanced clinical stage, and low dietary diversity. CONCLUSIONS: One in every four pre-ART PLWHIV presented with undernutrition in Dar es salaam, Tanzania. Risk factors for undernourishment included younger age, lower household income, advanced HIV clinical stage, and lower dietary diversity score. Knowledge of the prevalence and prevailing risk factors for undernutrition among pre-ART PLWHIV should guide targeted, early integration of nutrition interventions into routine HIV care and treatment in high-prevalence, low-income settings such as Tanzania.

The level of APOBEC3G (hA3G)-related G-to-A mutations does not correlate with viral load in HIV type 1-infected individuals.

The APOBEC family of mammalian cytidine deaminases, such as APOBEC3G (hA3G), has been demonstrated to function as a host viral restriction factor against HIV-1. hA3G has been shown to cause extensive G-to-A mutations in the HIV-1 genome, which may play a role in viral restriction. To investigate the role of G-to-A mutations in HIV-1 pathogenesis, we isolated, amplified, and sequenced HIV-1 sequences (vif, gag, and env) from 29 therapy-naive HIV-1-infected individuals. The levels of G-to-A mutations correlated with the expression levels of hA3G in the vif (rho = 0.438, p = 0.041) and the env regions (rho = 0.392, p = 0.038), but not in the gag region (rho = 0.131, p = 0.582). There is no correlation between viral load and the level of G-to-A mutations in the vif (rho = 0.144, p = 0.522), env (rho = 0.168, p = 0.391), or gag regions (rho = -0.254, p = 0.279). Taken together, these findings suggest that the hA3G-induced G-to-A mutations may not be the mechanism by which hA3G restricts or controls viral replication. Thus, hA3G might be restricting viral growth in infected individuals through a mechanism that is independent of the cytidine deaminase activities of hA3G.

Relationship between human immunodeficiency type 1 infection and expression of human APOBEC3G and APOBEC3F.

BACKGROUND: Human immunodeficiency virus type 1 (HIV-1)-infected individuals with a high viral set point progress to acquired immunodeficiency syndrome (AIDS) more rapidly than those with a low viral set point. It is not entirely clear which host and viral factors are responsible for the viral set point. Host factors that affect virus replication are likely to influence the viral set point. Human APOBEC proteins have been shown to restrict HIV-1 replication. METHODS: This prospective study was conducted to determine the relationship between human APOBEC3G (hA3G) and APOBEC3F (hA3F) levels and the viral set point. Fourteen subjects were classified as having a high viral set point, and 16 were classified as having a low viral set point. We quantified the levels of hA3G and hA3F mRNA in HIV-1-infected, antiretroviral drug-naive individuals before and after infection. RESULTS: We found a significant correlation between the hA3G mRNA level and the viral set point. The expression of hA3G and hA3F increased after infection, and the levels of hA3G and hA3F mRNA were significantly higher after infection in the low viral set point group, compared with the high viral set point group. CONCLUSIONS: The results suggest that the level of hA3G expression affects the establishment of the viral set point and may therefore function as a host determinant in the pathogenesis of HIV-1 infection.