The occurrence of

The impact of Structured Treatment Interruption (STI) in peripheral blood mononuclear cell (PBMC) proviral reservoirs in 41 highly active antiretroviral therapy (HAART)-treated viremic individuals at baseline and 12 weeks after STI was determined using quantitative PCR (qPCR). Viral load increased 0.7 log 10 and CD4 decreased 97.5 cells/mm 3 after 12 weeks. A total of 28 of the 41 individuals showed an increased proviral load, 19 with a statistically significant increase above 10%. An increase in active viral replication is an important factor in the replenishment of the proviral reservoir even for short time periods.

We analyzed gp120V3 HIV-1 env region genetic diversity of 27 patients failing antiretrovirals and subjected to 12-week structured treatment interruption (STI). Based on heteroduplex mobility assays, eight patients presented low pre- and post-STI genetic diversity (G1); five presented high pre-STI but low post-STI diversity (G2); five presented low pre-STI and high post-STI diversity (G3); and nine, high pre- and post-STI diversity (G4). One patient from G1, two from G2 and two from G3 were subjected to proviral DNA end-point PCR and sequencing. In three patients, the dramatic disturbance caused by STI resulted in ancestral viral progeny activation, which repopulated the cell reservoir. In two patients presenting highly homogeneous sequences and low immune selective pressure (dN/dS ratio <1), this phenomenon was not observed. The mechanisms involved in viral evolution, in which antiretroviral therapy also applies selective pressure, sometimes affects coreceptor usage of circulating viruses, leading to the suppression of x4 strains.

A seroepidemiological study was carried out from 1992 to 1993 to estimate the prevalence of antibody to prevailing influenza virus strains circulating among patients attending the IEC Virology Laboratory in Belem, Northern Brazil. A total of 179 (11%) of serum samples were obtained during the post-epidemic period and processed by the hemagglutination inhibition test against the A/Taiwan/1/86 (H1N1), A/Beijing/353/89 (H3N2), and B/Yamagata/16/88 types of influenza virus. The serological results indicate circulation of viruses antigenically related to all three strains during the two-year study period. In 1992, the overall prevalence rates of HI antibodies to H1N1 and H3N2 were 84% and 56%, respectively. Presence of antibodies to both strains was detected in all age groups, suggesting intense viral activity that year. Antibodies to influenza B were detected at lower levels in all patients during this period. Similar prevalence to the H1N1 virus was noted in 1993, indicating that this strain occurred in both years. However, an increase in prevalence rates for the H3N2 virus was seen in 1993, suggesting that this strain (or a related virus) circulated intensively during this year. Influenza B activity also increased in 1993, causing infection mainly among young adults.

HIV cure studies require patients to enter an analytical treatment interruption (ATI). Here, we describe previously unanalyzed data that sheds light on ATI dynamics in PLHIV (People Living with HIV). We present drug resistance mutation dynamics on the pol gene among individuals with antiretroviral virological failure who underwent ATI. The study involved a 12-week interruption in antiretroviral therapy (ART), monitoring of viral load, CD4+/CD8+ T cell counts, and sequencing of the pol gene from 38 individuals experiencing virological failure and harboring 3-class resistant HIV strains: nucleoside reverse transcriptase inhibitors (NRTI) non-nucleoside inhibitors (NNRTI), and protease inhibitors (PI). Protease and reverse transcriptase regions of the pol gene were sequenced at baseline before ATI and every four weeks thereafter from PBMCs and at baseline and after 12 weeks from plasma HIV RNA using population-based Sanger sequencing. Average viral load increased 0.559 log10 copies per milliliter. CD4+ T cell count decreased as soon as ART was withdrawn, an average loss of 99.0 cells/mL. Forty-three percent of the mutations associated with antiretroviral resistance in PBMCs disappeared and fifty-seven percent of the mutations in plasma reverted to wild type, which was less than the 100% reversion expected. In PBMC, the PI mutations reverted more slowly than reverse transcriptase mutations. The patients were projected to need an average of 33.7 weeks for PI to revert compared with 20.9 weeks for NRTI and 19.8 weeks for NNRTI. Mutations in the pol gene can cause virological failure and difficulty in re-establishing effective virological suppression.