Zika virus (ZIKV) persists in the semen of male patients, a first for flavivirus infection. Here, we demonstrate that ZIKV can induce inflammation in the testis and epididymidis, but not in the prostate or seminal vesicle, and can lead to damaged testes after 60 days post-infection in mice. ZIKV induces innate immune responses in Leydig, Sertoli, and epididymal epithelial cells, resulting in the production of pro-inflammatory cytokines/chemokines. However, ZIKV does not induce a rapid and abundant cytokine production in peritubular cell and spermatogonia, suggesting that these cells are vulnerable for ZIKV infection and could be the potential repositories for ZIKV. Our study demonstrates a correlation between ZIKV and testis infection/damage and suggests that ZIKV infection, under certain circumstances, can eventually lead to male infertility.

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Background: This meta-analysis aimed to estimate the association of human immunodeficiency virus (HIV) infection and risk of coronavirus disease 2019 (COVID-19) mortality. Methods: We systematically retrieved articles published on HIV infection and risk of COVID-19 mortality through PubMed, EMBase, China National Knowledge Infrastructure, WanFang, and Chongqing VIP databases using a predefined search strategy from December 1, 2019 to January 31, 2021. Newcastle–Ottawa Scale (NOS) was used to assess the quality of the included studies. Cochran Q test and I 2 statistics were quantified to measure heterogeneity. Odds ratio (OR) and 95% confidence intervals (CI) were computed and displayed in the form of forest plots. Subgroup analysis was performed to explore the source of heterogeneity. Funnel plot, Begg test, and Egger test were used to assess potential publication bias. Stata software version 11.0 was used to analyze all the statistical data. Results: We included 10 studies with 18,122,370 COVID-19 patients, of whom 41,113 were with HIV infection and 18,081,257 were without HIV infection. The pooled overall results suggested that people living with HIV infection had a higher risk of mortality from COVID-19 than those without HIV infection (OR = 1.252, 95% CI 1.027–1.524). Subgroup analysis showed that people living with HIV infection had a higher risk of COVID-19 mortality than those without HIV infection in the United States (OR = 1.520, 95% CI 1.252–1.845) and in South Africa (OR = 1.122, 95% CI 1.032–1.220); however, no significant association was found in the United Kingdom (OR = 0.878, 95% CI 0.657–1.174). Conclusion: Patients with HIV infection should be the emphasis population to prevent the risk of mortality during the clinical treatment of COVID-19 patients.

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P2X7 receptor (P2X7R) is highly expressed on immune cells, triggering the release of cytokines and regulating autoimmune responses. To investigate P2X7R surface expression on T helper (Th) 1, Th17, and regulatory T (Treg) cells in patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA) and correlations with disease activity, 29 SLE and 29 RA patients and 18 healthy controls (HCs) were enrolled. We showed that SLE and RA patients had significantly higher levels of plasma cytokines (IFN-g, IL-1b, IL-6, IL-17A, and IL-23), frequencies of Th1 and Th17 cells, and expression of P2X7R on Th1 and Th17 than HCs, and the Th17/Treg ratio was significantly increased, whereas Treg cell levels were significantly decreased. The Ca 2+ influx increase following BzATP stimulation was significantly higher in CD4 + PBMCs from SLE and RA patients than in HCs. Blood levels of shed P2X7R were increased in SLE and RA patients. Furthermore, 28-joint Disease Activity Score and SLE Disease Activity Index score showed negative correlations with Treg cell levels and positive correlations with Th17/Treg ratio and Th17 cell P2X7R expression. Interestingly, Th17 cell P2X7R expression was closely correlated with IL-1b, C-reactive protein, the erythrocyte sedimentation rate, anticyclic citrullinated peptide Abs, albumin, and C4. These data indicate that increased Th17 cell P2X7R expression is functionally and positively related to disease activity and some inflammatory mediators in SLE and RA patients, and P2X7R could be critical in promoting the Th17 immune response and contributing to the complex pathogenesis of SLE and RA.