Detection Analysis and Study of Genomic Region Variability of JCPyV, BKPyV, MCPyV, HPyV6, HPyV7 and QPyV in the Urine and Plasma of HIV-1-Infected Patients

Abstract

Since it was clearly established that HIV/AIDS predisposes to the infection, persistence or reactivation of latent viruses, the prevalence of human polyomaviruses (HPyVs) among HIV-1-infected patients and a possible correlation between HPyVs and HIV sero-status were investigated. PCR was performed to detect and quantify JCPyV, BKPyV, MCPyV, HPyV6, HPyV7 and QPyV DNA in the urine and plasma samples of 103 HIV-1-infected patients. Subsequently, NCCR, VP1 and MCPyV LT sequences were examined. In addition, for MCPyV, the expression of transcripts for the LT gene was investigated. JCPyV, BKPyV and MCPyV’s presence was reported, whereas HPyV6, HPyV7 and QPyV were not detected in any sample. Co-infection patterns of JCPyV, BKPyV and MCPyV were found. Archetype-like NCCRs were observed with some point mutations in plasma samples positive for JCPyV and BKPyV. The VP1 region was found to be highly conserved among these subjects. LT did not show mutations causing stop codons, and LT transcripts were expressed in MCPyV positive samples. A significant correlation between HPyVs’ detection and a low level of CD4+ was reported. In conclusion, HPyV6, HPyV7 and QPyV seem to not have a clinical relevance in HIV-1 patients, whereas further studies are warranted to define the clinical importance of JCPyV, BKPyV and MCPyV DNA detection in these subjects.

MicroRNA dysregulations in Merkel cell carcinoma: Molecular mechanisms and clinical applications

“…3 Despite exhibiting similar symptomatology, two distinct MCC etiologies have been identified. 4,5 Nearly 80% of MCC cases are caused by a DNA tumor virus named Merkel cell polyomavirus (MCPyV), 6 that is, MCPyV-positive MCC (MCCP). 7 The remaining MCCs result as MCPyV-negative (MCCN).…”

Polyomavirus Wakes Up and Chooses Neurovirulence

“…Although JCPyV infects the kidney, the brain is typically the site of pathology, so the virus must travel between the organs. In patients with PML, the JCPyV in the brain is genotypically different from the virus in the kidney [ 21 , 27 , 125 , 126 , 127 , 128 , 129 , 130 ]. Polyomaviruses residing in the kidney typically exhibit the archetype strain.…”

“…Viral shedding increases and results in lytic infection. Patient studies have shown that the NCCR undergoes rearrangements in two human immunodeficiency virus (HIV)-positive patients with PML [ 127 , 134 , 135 ]. One study found that HIV-negative MS patients with PML did not have complex rearrangements, suggesting that either T helper cell depletion or HIV itself may play a role in NCCR rearrangement [ 29 ].…”