Monolateral Ocular Tuberculosis in an Immunocompetent Patient: A Case Report

Abstract Introduction -A rare case of monolateral tubercular choroiditis in a 25 year old Bengali man without pulmonary involvement was reported

Brief report: L-selectin (CD62L) is downregulated on CD4+ and CD8+ T lymphocytes of HIV-1-infected individuals naive for ART

The expression of L-selectin (CD62L) in HIV-1 infection has not been extensively investigated. Here, we measured CD62L expression on T-cell subsets of HIV-1-infected individuals naive for antiretroviral therapy (ART-naive) or receiving therapy (ART), and seronegative control subjects (HIV-neg). We found reduced frequencies of CD62L cells among CD4 and CD8 T cells from ART-naive as compared with ART and HIV-neg groups, particularly within naive and central memory subsets. CD62L expression on T cells inversely correlated with viral load and rapidly increased after ART initiation. Plasma sCD62L levels did not correlate with CD62L expression, being higher in all HIV-1-infected individuals as compared with HIV-neg subjects. Finally, CD62L downregulation was found associated with the expression of the CD38 activation marker in CD8 T cells, but not in CD4 T cells. We suggest that CD62L downregulation due to unconstrained HIV-1 replication may have important consequences for T-cell circulation and function and for disease progression

Expression and Function of NKG2D Is Impaired in CD8+ T Cells of Chronically HIV-1-Infected Patients Without ART

Increasing line of evidence indicates that the NKG2D-activating receptor plays a relevant role in the effector functions of cytotoxic lymphocytes. In this study, we investigated the expression and function of NKG2D in CD8⁺ T cells from chronically HIV-1-infected patients with or without antiretroviral therapy (ART)

Viral growth assay to evaluate the replicative capacity of HIV-1 isolates

The replicative capacity of HIV is studied by carrying out replication-competition experiments with the insertion of the gene of interest. These assays cannot capture the complicated patterns of mutations of different genes. A cross sectional study was carried out on 10 HIV-infected naive patients and on 15 patients failing HAART. The CD8-depleted PBMCs, with known proviral DNA and cellular HIV-RNA copy numbers, were cultured. A reference curve was determined using the data obtained from 10 naive patients. The replicative capacity was calculated as the ratio multiplied by 100 of the p24 antigen level of isolates over the p24 antigen level determined on the reference curve. A linear correlation between p24 antigen level and the infectious doses of HIV-DNA alone or plus cellular RNA copy number of PBMCs was found in naive patients (r = 0.63, P < 0.001 and r = 0.67, P < 0.001, respectively). Although all patients failing therapy had strains with impaired replicative capacity, a wide range of values (0.1-74.5%) was detected. All strains with a replicative capacity above 10% had non-nucleoside reverse transcriptase inhibitors related mutations. A viral assay to evaluate the HIV replicative capacity is described. The high variability of replicative capacity confirms the need to undertake replicative capacity assay using the whole virus. (C) 2003 Elsevier B.V. All rights reserved

Decrease of replicative capacity of HIV isolates after genotypic guided change of therapy

A longitudinal study of the replication capacity of HIV strains isolated from 18 patients failing highly active antiretroviral therapy (HAART) was undertaken at the time of genotypic guided change of therapy and after 12 months. Patients were divided in two groups according to the response to therapy: immune responders (12 patients with immune recovery defined as having more than 100 CD4 cells compared to baseline value), and failing patients (six patients without immune recovery). At enrollment no significant difference in terms of CD4 cell count and HIV plasma viremia was detected between the two groups. One year after change of therapy, all patients experienced a decrease in the replication capacity of HIV strains. The HIV replication capacity of the failing and of immune-responder patients decreased from 60% (range 14-96%) to 26.4% (range 0.4-74.5) and from 46.8% (range 15-98%) to 3.6% (range 0.1-26.8%), respectively. At month 12, the difference of HIV replication capacity between the two groups reached a statistical significance (P<0.03). After the change of therapy, an increase in the number of drug resistance mutations in the protease gene was detected in both groups with a higher prevalence of M36I mutation in immune responders. The HIV strains of patients failing HAART showed a progressive impaired replication capacity. The degree of the impairment in viral replication correlated with the viro-immunological discordant response to HAART and with the acquisition of new drug resistant mutations in the protease gene. In patients failing HAART, the impaired replication capacity of HIV strains could justify the persistence of an immune recovery