HIV-1 persists in cellular reservoirs that can reignite viremia if antiretroviral therapy (ART) is interrupted. Therefore, insight into the nature of those reservoirs may be revealed from the composition of recrudescing viremia following treatment cessation. A minor population of macrophage-tropic (M-tropic) viruses was identified in a library of recombinant viruses constructed with individual envelope genes that were obtained from plasma of six individuals undergoing analytic treatment interruption (ATI). M-tropic viruses could also be enriched from post-ATI plasma using macrophage-specific (CD14) but not CD4+ T cell-specific (CD3) antibodies, suggesting that M-tropic viruses had a macrophage origin. Molecular clock analysis indicated that the establishment of M-tropic HIV-1 variants predated ATI. Collectively, these data suggest that macrophages are a viral reservoir in HIV-1–infected individuals on effective ART and that M-tropic variants can appear in rebounding viremia when treatment is interrupted. These findings have implications for the design of curative strategies for HIV-1.

HIV-1 has evolved mechanisms to evade host cell immune responses and persist for lifelong infection. Latent cellular reservoirs are responsible for this persistence of HIV-1 despite the powerful effects of highly active antiretroviral therapies (HAART) to control circulating viral load. While cellular reservoirs have been extensively studied, much of these studies have focused on peripheral blood and resting memory CD4+ T cells containing latent HIV-1 provirus; however, efforts to eradicate cellular reservoirs have been stunted by reservoirs found in tissues compartments that are not easily accessible. These tissues contain resting memory CD4+ T cells and tissue resident macrophages, another latent cellular reservoir to HIV-1. Tissue resident macrophages have been associated with HIV-1 infection since the 1980s, and evidence has continued to grow regarding their role in HIV-1 persistence. Specific biological characteristics play a vital role as to why macrophages are latent cellular reservoirs for HIV-1, and in vitro and in vivo studies exhibit how macrophages contribute to viral persistence in individuals and animals on antiretroviral therapies. In this review, we characterize the role and evolutionary advantages of macrophage reservoirs to HIV-1 and their contribution to HIV-1 persistence. In acknowledging the interplay of HIV-1 and macrophages in the host, we identify reasons why current strategies are incapable of eliminating HIV-1 reservoirs and why efforts must focus on eradicating reservoirs to find a future functional cure.

We found a robust association between phimosis and the genital HPV prevalence in men and a significant frequency of high risk HPV. Other studies are needed to investigate the occurrence of factors that can increase the incidence of penile carcinoma and determine its impact on female genital infection in cervical cancer.

Little is known about penile carcinogenesis. The aim of this study was to evaluate the prevalence of HPV and EBV, and the methylation status of p16 in penile cancer samples, and to contribute to the understanding of the mechanisms responsible for penile cancer development. HPV DNA was detected in 63.6% of 122 cases, with HPV16 being the most prevalent type. EBV DNA was detected in 47.7%, with EBV-1 being the most prevalent type. HPV/EBV co-infections were found in 27.3% of the cases. Hypermethylation in p16 was detected in 64.5% of 110 tested cases. An association between the absence of HPV absence and p16 hypermethylation was also found. Death and/or progressive disease was associated with grade (P = 0.001), T stage (P < 0.0001), and N stage (P < 0.0001). In the multivariable model, grade and N stage were independent risk factors for disease-free survival (P = 0.008 and P < 0.001, respectively). Patients without viral infection had a median age significantly lower than that of the HPV-infected patients. We suggest at least two pathways for penile carcinogenesis, one HPV-independent linked to epigenetic events, probably via p16 inactivation; and another, dependent on HPV infection.

Introduction: Genital infections by human papillomavirus (HPV) are the most prevalent sexually transmitted viral diseases worldwide. Although the natural history of cervical cancer is better understood, there are still scarce information regarding the etiology of penile cancer, and the natural history of HPV infection in men is not yet fully elucidated. Objective: This study aimed to determine the prevalence of HPV infection in penile samples, from a clinically asymptomatic male population. Methods: A total of 550 samples were collected between January 2011 and July 2014 in different institutions in the State of Rio de Janeiro, including a dermatology clinic and a metallurgical company. The samples were collected from the anatomical regions of the glans and balanopreputial sulcus. HPV identification was made through the generic and type-specific Polymerase Chain Reaction (PCR), and Restriction Fragment Length Polymorphism (RFLP) techniques. Results: An overall prevalence of HPV infection was observed in 21.8% (120 subjects). The most prevalent HPV type was HPV 6 (35%), followed by HPV 16 (20.8%), HPV 11 (19.1%), HPV 31 (6.7%), HPV 33 (6.7%), HPV 45 (8.3%) and HPV 58 (3.3%). Hence, infection was associated with low-risk oncogenic types in 54.1% of the studied individuals, while high-risk oncogenic types were detected in 45.9% of them. The age of the studied subjects ranged from 18 to 65 years with a mean age of 28.4 years. Conclusion: According to our findings, we can infer that the prevalence of HPV infection among asymptomatic male population was considerably lower than the described in the literature, although in agreement with results reported in some recently published studies. We believe that the results may contribute to understand the features of circulation of HPV in male population, in order to evaluate risk-benefits and strategies of disease prevention.