The presence of transmitted drug resistance (TDR) in treatment-naive HIV-1-positive subjects is of concern, especially in the countries of the former Soviet Union in which the number of subjects exposed to antiretrovirals (ARV) has exponentially increased during the past decade. We assessed the rate of TDR among newly diagnosed subjects in Estonia in 2010 and compared it to that in 2008. The study included 325 subjects (87% of all subjects tested HIV positive from January 1 to December 31, 2010). Of the 244 sequenced viral genomic RNA in the reverse transcriptase (RT) region 214 were CRF06_cpx, nine were subtype A1, three (one each) were subtype B and subtype C, CRF02_AG, and CRF03_AB; 15 viruses remained unclassified as putative recombinant forms between CRF06_cpx and subtype A1. HIV-1 TDR mutations in 2010 and 2008 (n=145) occurred at similar frequency in 4.5% (95% CI 2.45; 7.98) and 5.5% (95% CI 1.8; 9.24) of the patients, respectively. In 2010, 2.5% (6/244) of the sequences harbored nonnucleoside reverse transcriptase inhibitor (NNRTI) (K103N and K101E), 1.6% (4/244) nucleoside reverse transcriptase inhibitor (NRTI) (M41L, M184I, and K219E), and 0.4% (1/244) protease inhibitor (PI) (V82A) mutations. Our findings indicate that in spite of the increased consumption of ARVs the rate of TDR in Estonia has remained unchanged over the past 3 years. Similar stabilizing or even decreasing trends have been described in Western Europe and North America albeit at higher levels and in different socioeconomic backgrounds.
Intravenous drug use (IDU) is one of the most important transmission routes for blood borne viruses, including human immunodeficiency virus (HIV), hepatitis B virus (HBV), and hepatitis C virus (HCV). These infections alter the subset distributions of T cells; however, knowledge of such effects during HIV, HBV, and or HCV coinfection is limited. Therefore, we aimed to evaluate any associations between T cell distribution and the presence of HIV, HBV, and HCV coinfections among persons who inject drugs (PWID). Blood samples from 88 Caucasian PWID (mean age 30; 82% male) and 47 age-matched subjects negative for all three infections (mean age of 29; 83% male) were analyzed. The T cell markers CD3, CD4, CD8, CD45RA, CCR7, HLA-DR, and CCR5 were assessed using flow cytometry. Of the PWID, 40% were HIV+HBV+HCV+, 20% HBV+HCV+, 19% HCV+, and 13% negative for all three infections. The HIV+HBV+HCV+ PWID had lower percentages of CD4 + and higher percentages of CD8 + cells compared to triple negative PWID ( p < 0.001 in all cases). The only difference between HBV+HCV+ with triple negative PWID was the lower CD4 + cell percentages among the former (52.1% and 58.6%, p = 0.021). Triple negative PWID had higher immune activation and number of CCR5+ cells compared to the controls. We suggest that the altered T cell subset distribution among PWID is mainly triggered by HIV infection and or IDU, while HBV and or HCV seropositivity has minimal additional effects on CD4 + cell distribution.
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