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Background SARS-CoV-2 is a novel coronavirus and the cause of COVID-19. More than 80% of COVID-19 patients exhibit mild or moderate symptoms. In this study, we investigated the dynamics of viral load and antibodies against SARS-CoV-2 in a longitudinal cohort of COVID-19 patients with severe and mild/moderate diseases. Methods Demographic and clinical information were obtained. Serial samples of blood, nasal and pharyngeal and anal swabs were collected at different time points post-onset. SARS-CoV-2 RNA and anti-SARS-CoV-2 antibodies were measured by qRT-PCR and immunoassays, respectively. Results Respiratory SARS-CoV-2 RNA was detectable in 58.0% (58/100) COVID-19 patients upon admission and lasted for a median of 13 days post-onset. In addition, 5.9% (1/17) and 20.2% (19/94) of the blood and anal swab specimens were positive for SARS-CoV-2 RNA, respectively. Anal viral RNA was more frequently detected in the patients who were positive for viral RNA in the respiratory samples upon admission. Specific anti-SARS-CoV-2 antibody developed within two weeks after onset, reached peak approximately 17 days post-onset and then maintained at relatively high level up to 50 days we analyzed in most patients. However, the levels of antibodies were variable among the patients. High titers of antibodies appeared to be associated with the severity of the disease. Furthermore, viral proteins from different sources showed significant difference of serological sensitivity especially during the first week post-onset. Conclusions Our results indicate rapid clearance or self-elimination of viral RNA in about half of the COVID-19 patients upon admission. Viral RNA shedding of SARS-CoV-2 occurred in multiple tissues including the respiratory system, blood, and intestine. Variable levels of specific anti-SARS-CoV-2 antibody may be associated with disease severity. These findings have shed light on viral kinetics and antibody response in COVID-19 patients and provide scientific evidence for infection control and patient management.

Background Men who have sex with men (MSM) are vulnerable risk group for human immunodeficiency virus (HIV)-1 infection. However, some MSM do not disclose their same-sex behavior and could impact the transmission and prevention of HIV-1 infection. Here, we evaluated the role of nondisclosed MSM in HIV-1 transmission in Guangzhou, China. Methods The HIV-1 pol sequences were obtained from HIV-infected subjects from 2008 to 2015. A transmission network was constructed using HIV TRAnsmission Cluster Engine (HIV-TRACE) at a pairwise genetic distance of 0.5%. The position of nondisclosed MSM in the network was determined by centrality analysis. Results Nondisclosed MSM were inferred in 9.92% (61 of 615) of slightly older, self-reported non-MSM (P = .006). They were more likely to be married (P = .002) and less educated (P < .001) than the MSM with whom they clustered. Closeness centrality was bigger for nondisclosed MSM than for MSM (P < .001), indicating the central position of nondisclosed MSM in the networks. The average shortest path length was smaller for nondisclosed MSM than for MSM (P < .001), whereas radiality was bigger for nondisclosed MSM than for MSM, suggesting a relatively greater contribution of nondisclosed MSM in transmitting HIV-1 than MSM. Assortativity analysis indicated that nondisclosed MSM were more likely to link each other with coefficient of 0.025. Conclusions Nondisclosed MSM are a specific group, and they play an important role in HIV-1 transmission. They could be bisexual and might increase the risk of HIV-1 infection to their sex partners. Therefore, specific prevention and intervention targeting nondisclosed MSM are urgently needed.

ObjectivesHIV-1 genetic diversity is increasing among men who have sex with men (MSM) in China, but the association of HIV-1 genotype with disease progression remains to be elucidated. MethodsWe collected data in an observational longitudinal cohort study of 860 HIV-1-infected MSM in Guangzhou, China between January 2008 and March 2017. Kaplan-Meier analysis and Cox proportional hazard model were used to predict the time from HIV-1 diagnosis to immunodeficiency progression (CD4 cell count < 200 cells/ll) as well as adjusted hazard ratio (aHR). ResultsCRF01_AE and HIV-1 subtype B infection were associated with higher percentage of patients progressed to immunodeficiency and higher incidence of immunodeficiency than infection with CRF07_BC or CRF55_01B. Compared with CRF07_BC, the time from HIV-1 diagnosis to immunodeficiency were different among the major HIV-1 genotypes, which ranked as follows, in descending order: CRF07_BC (7.03 years) > CRF55_01B (5.71 years, P = 0.014; aHR 3.752, P = 0.0923) > CRF01_AE (5.18 years, P < 0.001; aHR 4.733, P = 0.0152). HIV-1 genotype, viral load and baseline CD4 T-cell count were three independent variables associated with disease progression. ConclusionsOur results confirm differential rates of immunodeficiency progression as a function of HIV-1 genotype. The impact of HIV-1 genotype on HIV epidemics, patient management and prevention should be further investigated.

Background Chlamydia trachomatis is the most common sexually transmitted infection and the bacterial agent of trachoma globally. C. trachomatis undergoes a biphasic developmental cycle involving an infectious elementary body and a replicative reticulate body. Little is currently known about the gene expression dynamics of host cell mRNAs, lncRNAs, and miRNAs at different stages of C. trachomatis development. Results Here, we performed RNA-seq and miR-seq on HeLa cells infected with C. trachomatis serovar E at 20 h post-infection (hpi) and 44 hpi with or without IFN-γ treatment. Our study identified and validated differentially expressed host cell mRNAs, lncRNAs, and miRNAs during infection. Host cells at 20 hpi showed the most differential upregulation of both coding and non-coding genes while at 44 hpi in the presence of IFN-γ resulted in a dramatic downregulation of a large proportion of host genes. Using RT-qPCR, we validated the top 5 upregulated mRNAs and miRNAs, which are specific for different stages of C. trachomatis development. One of the commonly expressed miRNAs at all three stages of C. trachomatis development, miR-193b-5p, showed significant expression in clinical serum samples of C. trachomatis-infected patients as compared to sera from healthy controls and HIV-1-infected patients. Furthermore, we observed significant upregulation of antigen processing and presentation, and T helper cell differentiation pathways at 20 hpi whereas T cell receptor, mTOR, and Rap1 pathways were modulated at 44 hpi. Treatment with IFN-γ at 44 hpi showed the upregulation of cytokine-cytokine receptor interaction, FoxO signaling, and Ras signaling pathways. Conclusions Our study documented transcriptional manipulation of the host cell genomes and the upregulation of stage-specific signaling pathways necessary for the survival of the pathogen and could serve as potential biomarkers in the diagnosis and management of the disease.