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Background This study is the first to describe major epidemiological trends and clinical characteristics among Israeli men who have sex with men (MSM), who are at a higher risk for HIV infection. Methods This retrospective study includes all individuals reported to the Israeli Ministry of Health with HIV and self-identified as MSM between 1981 and 2015. The incidence rates of HIV infection and AIDS-defining diseases were analyzed and Kaplan-Meier survival estimates were calculated from time of HIV infection notification to AIDS diagnosis and death across three consecutive periods representing antiretroviral treatment availability. Results The trend of increase in HIV incidence is similar to Western Europe, although Israeli rates are lower. Of 2052 HIV/AIDS Israeli MSM diagnosed during the follow-up, 296 (14.6%) developed AIDS. MSM constitute 28.4% of all HIV/AIDS cases and 41.5% of cases among men. Average times from HIV-notification until AIDS diagnosis were 15.5 [14.0–16.9], 16.0 [15.5–16.4], and 6.7 [6.7–6.8] years, within 1981–1996, 1997–2007, and 2008–2015, respectively. The HIV-incidence rate among Israeli MSM slightly declined from 2012, after peaking in 2011 at 6.2 per 100,000. Conclusions The recent reduction in HIV-incidence and in AIDS diagnoses among Israeli MSM is encouraging. Nevertheless, the disproportionate incidence of HIV among MSM requires sustained efforts to abate further infections.

Report of an acquired immunodeficiency syndrome (AIDS) patient with Epstein-Barr virus (EBV)-associated iris smooth muscle tumor. A 14-year-old African American female diagnosed with AIDS developed a painless iris mass in the right eye for 10 months. Iridocyclectomy was performed, and the pathology indicated EBV-associated iris smooth muscle tumor with epithelioid morphology. Immunohistochemical stains and in situ hybridization for EBV-encoded ribonucleic acid are very useful diagnostic tools for definite diagnosis. At 14-month follow-up, the patient did not have any tumor recurrence. This is the case report of EBV-associated iris smooth muscle tumor in a person diagnosed with AIDS with a unique epithelioid morphologic feature.

Many species of African nonhuman primates are naturally infected with simian immunodeficiency viruses (SIVs) in the wild and in captivity. In contrast to HIV-infected humans, these natural SIV hosts typically do not develop AIDS, despite chronic infection with a highly replicating virus. In this Review, we discuss the most recent advances on the mechanisms of protection from disease progression in natural SIV hosts, with emphasis on how they differ from pathogenic HIV/SIV infections of humans and rhesus macaques. These mechanisms include: (i) resolution of immune activation after acute infection, (ii) restricted pattern of target cell infection, and (iii) protection from mother-to-infant transmission. We highlight the areas that should be pursued in future studies, focusing on potential applications for the treatment and prevention of HIV infection.

The progressive depletion of quiescent \"bystander\" CD4 T cells, which are nonpermissive to HIV infection, is a principal driver of the acquired immunodeficiency syndrome (AIDS). These cells undergo abortive infection characterized by the cytosolic accumulation of incomplete HIV reverse transcripts. These viral DNAs are sensed by an unidentified host sensor that triggers an innate immune response, leading to caspase-1 activation and pyroptosis. Using unbiased proteomic and targeted biochemical approaches, as well as two independent methods of lentiviral short hairpin RNA–mediated gene knockdown in primary CD4 T cells, we identify interferon-γ–inducible protein 16 (IFI16) as a host DNA sensor required for CD4 T cell death due to abortive HIV infection. These findings provide insights into a key host pathway that plays a central role in CD4 T cell depletion during disease progression to AIDS.

We describe a case of a 57-year-old Caribbean-Black male with a medical history of concealed human immunodeficiency virus/acquired immunodeficiency syndrome who presented with cardiac tamponade (CT) secondary to disseminated histoplasmosis. The patient underwent emergent pericardiocentesis with immediate normalization of his hemodynamic status and resolution of obstructive shock. The clinician should consider atypical etiologies of CT, such as opportunistic infections in patients with HIV/AIDS.

Evidence of simian immunodeficiency virus (SIV) infection has been reported for 26 different species of African nonhuman primates. Two of these viruses, SIVcpz from chimpanzees and SIVsm from sooty mangabeys, are the cause of acquired immunodeficiency syndrome (AIDS) in humans. Together, they have been transmitted to humans on at least seven occasions. The implications of human infection by a diverse set of SIVs and of exposure to a plethora of additional human immunodeficiency virus-related viruses are discussed.

Spontaneous control of chronic-phase HIV/SIV viremia is often associated with the expression of specific MHC class I allotypes. HIV/SIV-specific CD8+ cytotoxic T lymphocytes (CTLs) restricted by these MHC class I allotypes appear to be critical for viremic control. Establishment of the elite controller (EC) phenotype is predictable in SIVmac239-infected Indian rhesus macaques (RMs), with approximately 50% of + RMs and 20% of + RMs becoming ECs. Despite extensive characterization of EC-associated CTLs in HIV/SIV-infected individuals, the precise mechanistic basis of elite control remains unknown. Because EC and non-EC viral load trajectories begin diverging by day 14 post-infection, we hypothesized that hyperacute innate immune responses may contribute to viremic control. To gain insight into the immunological factors involved in the determination of EC status, we vaccinated 16 + RMs with Vif and Nef to elicit EC-associated CTLs, then subjected these 16 vaccinees and an additional 16 unvaccinated + controls to repeated intrarectal SIVmac239 challenges. We then performed whole-blood transcriptomic analysis of all 32 SIVmac239-infected + RMs and eight SIVmac239-infected RMs during the first 14 days of infection. Vaccination did not provide protection against acquisition, but peak and setpoint viremia were significantly lower in vaccinees relative to controls. We did not identify any meaningful correlations between vaccine-induced CTL parameters and SIVmac239 acquisition rate or chronic-phase viral loads. Ultimately, 13 of 16 vaccinees (81%) and 7 of 16 controls (44%) became ECs (viremia ≤ 10,000 vRNA copies/mL plasma for ≥ 4 weeks). We identified subsets of immunomodulatory genes differentially expressed (DE) between RM groupings based on vaccination status, EC status, and MHC class I genotype. These DE genes function in multiple innate immune processes, including the complement system, cytokine/chemokine signaling, pattern recognition receptors, and interferon-mediated responses. A striking difference in the kinetics of differential gene expression among our RM groups suggests that -associated elite control is characterized by a robust, rapid innate immune response that quickly resolves. These findings indicate that, despite the association between MHC class I genotype and elite control, innate immune factors in hyperacute SIV infection preceding CTL response development may facilitate the establishment of the EC phenotype.

HIV emerged following cross-species transmissions of simian immunodeficiency viruses (SIVs) that naturally infect non-human primates (NHPs) from Africa. While HIV replication and CD4 + T-cell depletion lead to increased gut permeability, microbial translocation, chronic immune activation, and systemic inflammation, the natural hosts of SIVs generally avoid these deleterious consequences when infected with their species-specific SIVs and do not progress to AIDS despite persistent lifelong high viremia due to long-term coevolution with their SIV pathogens. The benign course of natural SIV infection in the natural hosts is in stark contrast to the experimental SIV infection of Asian macaques, which progresses to simian AIDS. The mechanisms of non-pathogenic SIV infections are studied mainly in African green monkeys, sooty mangabeys, and mandrills, while progressing SIV infection is experimentally modeled in macaques: rhesus macaques, pigtailed macaques, and cynomolgus macaques. Here, we focus on the distinctive features of SIV infection in natural hosts, particularly (1): the superior healing properties of the intestinal mucosa, which enable them to maintain the integrity of the gut barrier and prevent microbial translocation, thus avoiding excessive/pathologic immune activation and inflammation usually perpetrated by the leaking of the microbial products into the circulation; (2) the gut microbiome, the disruption of which is an important factor in some inflammatory diseases, yet not completely understood in the course of lentiviral infection; (3) cell population shifts resulting in target cell restriction (downregulation of CD4 or CCR5 surface molecules that bind to SIV), control of viral replication in the lymph nodes (expansion of natural killer cells), and anti-inflammatory effects in the gut (NKG2a/c + CD8 + T cells); and (4) the genes and biological pathways that can shape genetic adaptations to viral pathogens and are associated with the non-pathogenic outcome of the natural SIV infection. Deciphering the protective mechanisms against SIV disease progression to immunodeficiency, which have been established through long-term coevolution between the natural hosts and their species-specific SIVs, may prompt the development of novel therapeutic interventions, such as drugs that can control gut inflammation, enhance gut healing capacities, or modulate the gut microbiome. These developments can go beyond HIV infection and open up large avenues for correcting gut damage, which is common in many diseases.

ObjectivesThe use of Highly Active Anti-Retroviral Therapy (HAART) as a treatment modality has led to an increase in the survival of people living with Human immunodeficiency virus (HIV) infection with accompanying overall increase in the frequency of some non-communicable diseases; particularly kidney diseases owing to drug toxicity, co-morbid chronic medical conditions and co-infection with other chronic viral illnesses.1 2 HIV infection is a known risk factor for kidney disease and Makurdi, Nigeria has a huge burden of the infection.3 This study determined the prevalence and risk factors of glomerular and proximal tubular dysfunction among children living with HIV attending tertiary health institutions in Makurdi, Nigeria.MethodsThis was a cross-sectional analytical study involving children aged 18 months to 17 years distributed into 91 children living with HIV and 91 age and sex-matched uninfected children for comparison. Relevant information was obtained from administered questionnaire and clinical records of these children. Blood samples for serum creatinine and urine samples for β2-microglobulin, albumin and creatinine were collected from each study participant. Data was analysed using SPSS version 23.0 and level of significance was taken as <0.05.ResultsThe prevalence of albuminuria was 65.9% (n = 60) among children living with HIV and 64.8% (n = 59) among comparison group (p = 0.876). The prevalence of reduced GFR was 5.5% (n = 5) among children living with HIV and 1.1% (n = 1) among the comparison group (p = 0.211).Table 1 shows overall prevalence of glomerular dysfunction was 4.4% (n = 4) among children living with HIV compared with 0% (n = 0) among comparison group (p = 0.115).Abstract 6425 Table 1Figure 1 shows prevalence of proximal tubular dysfunction was 93.4% (n = 85) among children living with HIV compared with 73.6% (n = 67) among comparison group (p = 0.001)Abstract 6425 Figure 1Prevalence of proximal tubular dysfunction among study participantsThe use of HAART for less than 60 months was identified as a risk factor for albuminuria [OR 2.69 (CI 1.040–6.958) p = 0.041]. Risk factors associated with reduced GFR were older age group [OR 0.670 (CI 0.513–0.876) p = 0.003], use of HAART for <60 months [OR 0.958 (CI 0.920 – 0.998), p = 0.038], and use of Tenofovir-based HAART regimen [OR 0.111 (CI 0–0.847) p = 0.032]. HIV infection was the only factor associated with proximal tubular dysfunction [OR 5.075 (CI 1.962 – 13.124) p = 0.001].ConclusionGlomerular and proximal tubular dysfunction are common among children living with HIV attending tertiary health institutions in Makurdi.ReferencesPhair J, Palella F. Renal disease in HIV infected individuals. Curr Opin HIV AIDS. 2011;6(4):285–28.Smith C, Sabin CA, Lundgren JD, Thiebaut R, Weber R, Law M, et al. Factors associated with specific causes of death amongst HIV-positive individuals in the D:A:D Study. AIDS. 2010;24(10):1537–1548.National Agency for the Control of HIV/AIDS (NACA). Nigeria Prevalence Rate. Available at: https://naca.gov.ng/nigeria-prevalence-rate/

Qualitative methods are not intrinsically progressive. Methods are simply tools to conduct research. Epistemology, the justification of knowledge, shapes methodology and methods, and thus is a vital starting point for a critical health equity research stance, regardless of whether the methods are qualitative, quantitative, or mixed. In line with this premise, I address four themes in this commentary. First, I criticize the ubiquitous and uncritical use of the term health disparities in U.S. public health. Next, I advocate for the increased use of qualitative methodologies—namely, photovoice and critical ethnography—that, pursuant to critical approaches, prioritize dismantling social–structural inequities as a prerequisite to health equity. Thereafter, I discuss epistemological stance and its influence on all aspects of the research process. Finally, I highlight my critical discourse analysis HIV prevention research based on individual interviews and focus groups with Black men, as an example of a critical health equity research approach.