Mechanisms underlying HIV-1 latency remain among the most crucial questions that need to be answered to adopt strategies for purging the latent viral reservoirs. Here we show that HIV-1 accessory protein Vpr induces depletion of class I HDACs, including HDAC1, 2, 3, and 8, to overcome latency in macrophages. We found that Vpr binds and depletes chromatin-associated class I HDACs through a VprBP-dependent mechanism, with HDAC3 as the most affected class I HDAC. De novo expression of Vpr in infected macrophages induced depletion of HDAC1 and 3 on the HIV-1 LTR that was associated with hyperacetylation of histones on the HIV-1 LTR. As a result of hyperacetylation of histones on HIV-1 promotor, the virus established an active promotor and this contributed to the acute infection of macrophages. Collectively, HIV-1 Vpr down-regulates class I HDACs on chromatin to counteract latent infections of macrophages.

HIV-1 Vpr is an accessory protein that induces proteasomal degradation of multiple proteins. We recently showed that Vpr targets class I HDACs on chromatin for proteasomal degradation. Here we show that Vpr induces degradation of HDAC1 and HDAC3 in HIV-1 latently infected J-Lat cells. Degradation of HDAC1 and HDAC3 was also observed on the HIV-1 LTR and as a result, markers of active transcription were recruited to the viral promoter and induced viral activation. Knockdown of HDAC1 and HDAC3 activated the latent HIV-1 provirus and complementation with HDAC3 inhibited Vpr-induced HIV-1 reactivation. Viral reactivation and degradation of HDAC1 and HDAC3 was conserved among Vpr proteins of HV-1 group M. Serum Vpr isolated from patients or the release of virion-incorporated Vpr from viral lysates also activated HIV-1 in latently infected cell lines and PBMCs from HIV-1 infected patients. Our results indicate that Vpr counteracts HIV-1 latency by inducing proteasomal degradation of HDAC1 and 3 leading to reactivation of the viral promoter.

Background:BK virus (BKV) belongs to the human Polyomaviridae and the primary BKV infection is occurred during childhood then the virus could be latent through life, especially in the kidneys and urinary system. It became reactive after an immunocompromised status, such as pregnancy or transplantation. Isolated BKV from different locations of the world is grouped into four subtypes using serological and genotyping methods. The BKV subtype I is the dominant one and has worldwide distribution.Objectives:According to our knowledge, there are no data about the BKV prevalence and its genotypes in southwest part of Iran. Considering the high prevalence of renal failure and kidney transplant patients in this part, and the role of BKV in graft rejection, this study aimed to determine the prevalence of BKV infection in renal transplant recipients referred to Golestan Hospital in Ahvaz City, Iran.Patients and Methods:Urine samples were collected from 122 kidney transplant recipients referred to Golestan Hospital in Ahvaz, southwest of Iran. The extracted DNA was amplified by Polymerase Chain Reaction, and subtype of each positive sample was determined using Restriction Fragment Length Polymorphism (RFLP) and sequencing methods.Results;From all study population, 51/122 (41.8%) urine samples were positive for BKV DNA and the other samples were negative (71/122). Forty-eight cases (94.11%) were subtype I and 3 others (5.89%) were subtype IV using the RFLP method. None of the patient’s urine samples were positive for subtypes II and III.Conclusions:Our work is the second study in Iran and considering huge numbers of transplantation in Iran and Khuzestan Province, south western of Iran, in addition to the role of this virus in kidney transplant rejection, routine evaluation of BKV positivity is recommended both for graft recipient and donors. This helps better transplantation result and may prevent graft rejection.

Background:Chronic rhinosinusitis (CRS) is one of the most common chronic illnesses, but the etiology and pathogenesis of CRS are not well understood. Few studies have been carried out on the role of viruses in patients with chronic sinusitis so far.Objectives:Regarding the high number of patients, we intended to evaluate the prevalence of rhinovirus and respiratory syncytial virus in patients with CRS. Doing so, we may pave the way for definitely achieving the causes and factors of the disease and consequently definite treatment of this debilitating disease in future studies.Patients and Methods:This cross-sectional study was carried out on 76 patients. Sample of the study consisted of patients with CRS who were candidates for functional endoscopic sinus surgery (FESS). The specimens were collected during FESS between February 2013 and December 2013. For this purpose, after entering into sinuses, the specimens were collected from their mucus. They were then placed in Dulbecco's modified Eagle's viral transport medium (DMEM). They were transferred to the virology lab of the university in a cold chain. The specimens were maintained in -70°C before examination. Reverse transcriptase-polymerase chain reaction (RT-PCR) was applied to explore the presence of rhinovirus and respiratory syncytial virus.Results:In this study, 76 patients with rhinosinusitis underwent FESS as qualified candidates. The sample of the study consisted of 48 males (63.2%) and 28 females (36.8%) with the mean age of 44.3 years and an age range of 19-76 years. Among the 76 patients, 53 were with polyps and 23 without polyps. Among the patients, 66 were candidates of FESS for the first time. Other 11 patients had previously undergone the surgery. The results from PCR indicated that 22 (28.94%) patients had rhinovirus and 9 (11.84%) had respiratory syncytial virus (RSV). A total of 25 patients (32.89%) had one of the two viruses. In 6 (7.89%) specimens, both viruses were reported.Conclusions:CRS is a common disease with negative effects on the quality of patients’ lives. This study showed the high prevalence of these two common respiratory viruses in patients with CRS.

Background:The human cytomegalovirus (HCMV) is a common pathogen which usually remains asymptomatic in the healthy adults; however, it can cause a symptomatic disease in the immunocompromised patients. The risk of infection with HCMV increases in ulcerative colitis (UC) patients as a result of receiving immunosuppressive agents.Objectives:This study aimed to determine the prevalence and the glycoprotein B genotypes of HCMV among the patients with HCMV disease superimposed on an UC flare that required hospitalization in Imam Khomeini Hospital in Ahvaz, Iran, during 2010- 2012.Patients and Methods:In this case-control study, formalin-fixed paraffin-embedded intestinal tissue samples were taken from 98 patients with UC disease including 53 males and 45 females (mean age ± standard deviation, 38.95 ± 17.93) and 67 control patients with noninflammatory disease who were referred to Imam Khomeini Hospital during 2010-2012. Detection of HCMV genome in intestinal samples was carried out by seminested polymerase chain reaction. Glycoprotein B genotypes were determined by sequencing.Results:Among 98 patients with UC, only 12 (12.2%) patients were positive for HCMV genome, while the HCMV genome was not detected in any of the controls. (P = 0.002). The distribution of HCMV gB genotypes in 12 CMV-positive UC patients was as follow: gB1, 11 (91.7%) and gB3, 1 (8.3%). The most prevalent genotype in CMV-positive UC patients was gB1.Conclusions:In this study, high prevalence of 91.7% HCMV gB1 genotype was predominant among HCMV-positive UC patients, which suggests that there might be an association between HCMV gB genotype 1 and UC disease.