METHODS: Data on children with perinatally acquired HIV aged <18 years on first-line, non-nucleoside reverse transcriptase inhibitor-based cART with viral suppression (two consecutive pVL <400 copies/mL over a six-month period) were included from a regional cohort study; those exposed to prior mono- or dual antiretroviral treatment were excluded. Frequency of pVL monitoring was determined at the site-level based on the median rate of pVL measurement: annual 0.75 to 1.5, and semi-annual >1.5 tests/patient/year. Treatment failure was defined as virologic failure (two consecutive pVL >1000 copies/mL), change of antiretroviral drug class, or death. Baseline was the date of the second consecutive pVL <400 copies/mL. Competing risk regression models were used to identify predictors of treatment failure.
RESULTS: During January 2008 to March 2015, there were 1220 eligible children from 10 sites that performed at least annual pVL monitoring, 1042 (85%) and 178 (15%) were from sites performing annual (n = 6) and semi-annual pVL monitoring (n = 4) respectively. Pre-cART, 675 children (55%) had World Health Organization clinical stage 3 or 4, the median nadir CD4 percentage was 9%, and the median pVL was 5.2 log10 copies/mL. At baseline, the median age was 9.2 years, 64% were on nevirapine-based regimens, the median cART duration was 1.6 years, and the median CD4 percentage was 26%. Over the follow-up period, 258 (25%) CLWH with annual and 40 (23%) with semi-annual pVL monitoring developed treatment failure, corresponding to incidence rates of 5.4 (95% CI: 4.8 to 6.1) and 4.3 (95% CI: 3.1 to 5.8) per 100 patient-years of follow-up respectively (p = 0.27). In multivariable analyses, the frequency of pVL monitoring was not associated with treatment failure (adjusted hazard ratio: 1.12; 95% CI: 0.80 to 1.59).
CONCLUSIONS: Annual compared to semi-annual pVL monitoring was not associated with an increased risk of treatment failure in our cohort of virally suppressed children with perinatally acquired HIV on first-line NNRTI-based cART.
METHODS: The study included 143 new cases of HIV-1 infection. Viral RNA was extracted from stocked plasma samples and sequenced for the pol and the env regions using the Sanger method. Near-full length sequencing using MiSeq was performed in 3 patients who were suspected to be infected with recombinant HIV-1. Phylogenetic analysis was performed using the neighbor-joining method and Bayesian Markov chain Monte Carlo method.
RESULTS: MSM was the main transmission route in the previous and current studies. However, heterosexual route showed a significant increase in recent years. Phylogenetic analysis documented three taxa; Mongolian B, Korean B, and CRF51_01B, though the former two were also observed in the previous study. CRF51_01B, which originated from Singapore and Malaysia, was confirmed by near-full length sequencing. Although these strains were mainly detected in MSM, they were also found in increasing numbers of heterosexual males and females. Bayesian phylogenetic analysis estimated transmission of CRF51_01B into Mongolia around early 2000s. An extended Bayesian skyline plot showed a rapid increase in the effective population size of Mongolian B cluster around 2004 and that of CRF51_01B cluster around 2011.
CONCLUSIONS: HIV-1 infection might expand to the general population in Mongolia. Our study documented a new cluster of HIV-1 transmission, enhancing our understanding of the epidemiological status of HIV-1 in Mongolia.