We investigated the distribution of HIV-1 subtypes and the prevalence of HIV-1 drug resistance among HIV-infected antiretroviral-naive patients in Guangxi, southern China. A total of 144 subjects from Liuzhou or Nanning, two cities having the most HIV-infected cases in Guangxi, were enrolled. HIV-1 pol fragments were amplified and sequenced from plasma of all patients. In all, 124 sequences were obtained, with 67 from Liuzhou and 57 from Nanning. All sequences were subtyped by phylogenetic analysis and analyzed for antiretroviral resistance using the HIVdb program. Our data showed that the sequences from Liuzhou were subtyped as CRF01_AE (77.6%), CRF07_BC(20.9%), and BC (1.5%), respectively, and the sequences from Nanning as CRF01_AE (78.9%), CRF08_BC (15.8%), B (3.5%), and C (1.8%), respectively. Of the sequences 11.9% from Liuzhou and 28.1% from Nanning harbored drug resistance-associated mutations, but there were only two sequences with mutations associated with significantly reduced phenotypic susceptibility to antiretroviral drugs.
Toll-like receptor 9 (TLR9) is one of the key sensors that recognize viral infection/replication in the host cells. Studies have demonstrated that methamphetamine (METH) dysregulated host cell innate immunity and facilitated HIV infection of macrophages. In this study, we present new evidence that METH suppressed TLR9-mediated anti-HIV activity in macrophages. Activation of TLR9 by its agonist CpG-ODN 2216 inhibits HIV replication, which was demonstrated by increased expression of TLR9, interferon (IFN)-α, IFN regulatory factor-7 (IRF-7), myeloid differentiation factor 88 (MyD88), and myxovirus resistance gene A (MxA) in macrophages. However, METH treatment of macrophages greatly compromised the TLR9 signaling-mediated anti-HIV effect and inhibited the expression of TLR9 downstream signaling factors. Dopamine D1 receptor (D1R) antagonists (SCH23390) could block METH-mediated inhibition of anti-HIV activity of TLR9 signaling. Investigation of the underlying mechanisms of the METH action showed that METH treatment selectively down-regulated the expression of TLR9 on macrophages, whereas it had little effect on the expression of other TLRs. Collectively, our results provide further evidence that METH suppresses host cell innate immunity against HIV infection by down-regulating TLR9 expression and its signaling-mediated antiviral effect in macrophages.
Background HIV self-testing (HIVST) is a potential strategy to overcome challenges of HIV testing among men who have sex with men (MSM). However, for resource-limited settings, technology and diagnostic devices are lagging. Hence, we estimated the status and correlates of HIVST among MSM in resource-limited settings in China to inform the development of HIVST to reach United Nations Programme on HIV and AIDS (UNAIDS) targets to end HIV by 2030. Methods A cross-sectional study was conducted among MSM in Nanning, Guangxi, China, between August 2019 and January 2020. The HIVST status was collected and data on social network features, sociodemographic information, risk behaviours, etc. were compared between prior- and non-HIVST MSM. Logistic regression analyses were conducted to examine the correlates of HIVST. Results The prevalence of HIVST among 446 MSM was 40.4% (95% confidence interval [CI] 35.8–44.9%). The main component of sociocentric network contains more prior-HIVST MSM (38.3%) than non-HIVST MSM (28.6%, P = 0.031). More MSM with individual features such as substance use during anal sex (22.8% vs 15.4%, P = 0.049) and multiple sexual partners (76.1% vs 59.4%, P < 0.001) were detected among prior-HIVST MSM. In multivariable analysis, prior HIVST was associated with the strong strength of ego-alter ties in the egocentric network (adjusted odds ratio [aOR] 1.72; 95% CI 1.09–2.71), HIV-infected partners (aOR, 7.17; 95% CI, 1.40–36.60), and vaginal intercourse (aOR, 0.38; 95% CI, 0.17–0.85). Conclusions HIVST coverage among MSM in resource-limited settings is suboptimal. Integrating social networks into testing services may be viable to promote HIVST in MSM within resource-limited settings.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.