Plague and "Anti-Quarantine" Writing in Traditional Chinese Biography

Quarantine remains important in treating infectious diseases in the world, but its legitimacy has frequently been questioned, not only during the COVID-19 pandemic but throughout world history - from Ancient Greece to Ancient China, from the past to the present. Anti-quarantine writings in traditional Chinese biography serve as a good example in this regard. They tend to "copy" from each other, since similar and repetitive narrative structures abound in these writings, usually to the neglect of the important dimensions, such as the medical knowledge and the psychological activities of the protagonists. The popularity of "anti-quarantine" writing in traditional Chinese biographies does not come from its literariness, and the biographies are mostly boring and full of cliches. What makes this writing popular is how it appeals to social realities and external factors such as politics, medicine, and ethics.

The impact of the Covid-19 pandemic on maternal delivery experiences and breastfeeding practices in China: data from a cross-sectional study.

BACKGROUND: The COVID-2019 pandemic has placed extensive pressure on health systems and posed a severe public health challenge worldwide. Lockdown measures implemented in many countries have delayed virus spread. However, a considerable number of people have faced unprecedented pressure, especially pregnant and breast-feeding women, because face-to-face professional support has been reduced during the lockdown in many countries. OBJECTIVES: To compare the delivery and infant feeding experiences of women who delivered before (BL) versus during (DL) the Covid-19 pandemic in Beijing, China and to investigate predictors of breastfeeding at 6-months. METHODS: Women aged ≥18 years with an infant ≤18 months of age completed an anonymous survey. Information/links were shared online and via local clinics in Beijing. Logistic regression was performed to assess predictors of breastfeeding during the first 6-months. RESULTS: One thousand eight hundred seven women provided data; BL 1231 (68.1%), DL 576 (31.9%). Significantly more mothers in DL group reported the lockdown had moderate to high impact to their household income (p = 0.013) and the convenience of purchasing daily necessities(p = 0.014). Compared to BL mothers, significantly more mothers in the DL groups thought their birth location and breastfeeding intention had been effected by the COVID-19 (p < 0.001, p = 0.036 respectively). Mostly breastfeeding (MBF, mainly breastfeeding with few non-formula fluids added) at 6 months was predicted by delivery during the lockdown period (OR1.43, 95% confidence interval (CI) 1.08, 1.90), younger maternal age (OR 0.96, 95%CI 0.93, 0.99), getting support from friends or relatives (OR 1.95, 95%CI 1.06, 3.59), and discussing health issues in online groups > four times a week (OR 1.66, 95%CI 1.09, 2.53). CONCLUSION: The COVID-19 pandemic and lockdown measures influenced mothers' planned birth location and breastfeeding intention. However, breastfeeding practice was maintained during the pandemic. Our results highlight the importance of feeding support as well as potential beneficial effects of increased mother-infant contact during the lockdown period which is relevant even under normal circumstances.

Maternal mental health and well-being during the COVID-19 pandemic in Beijing, China.

BACKGROUND: The aim of this study is to evaluate the impact of the coronavirus disease 2019 (COVID-19) pandemic on breastfeeding women and to identify predictors of maternal mental health and coping. METHODS: Mothers aged ≥ 18 years with a breast-fed infant ≤ 18 months of age during the COVID-19 pandemic in Beijing, China, completed a questionnaire. Descriptive analysis of lockdown consequences was performed and predictors of these outcomes were examined using stepwise linear regression. RESULTS: Of 2233 participants, 29.9%, 20.0% and 34.7% felt down, lonely, and worried, respectively, during the lockdown; however, 85.3% felt able to cope. Poorer maternal mental health was predicted by maternal (younger age, higher education) and infant (older age, lower gestation) characteristics, and social circumstances (husband unemployed or working from home, receiving advice from family, having enough space for the baby, living close to a park or green space). Conversely, better maternal mental health was predicted by higher income, employment requiring higher qualifications, more personal space at home, shopping or walking > once/week and lack of impact of COVID-19 on job or income. Mothers with higher education, more bedrooms, fair division of household chores and attending an online mother and baby group > once/week reported better coping. CONCLUSION: The findings highlight maternal characteristics and circumstances that predict poorer mental health and reduced coping which could be used to target interventions in any future public health emergencies requiring social restrictions.

SARS-CoV-2 ORF9b Antagonizes Type I and III Interferons by Targeting Multiple Components of RIG-I/MDA-5-MAVS, TLR3-TRIF, and cGAS-STING Signaling Pathways (preprint)

Severe acute respiratory syndrome corona-virus 2 (SARS-CoV-2), the etiologic agent of the coronavirus disease 2019 (COVID-19), has a catastrophic effect on human health and society. Clinical findings indicated that the suppression of innate antiviral immunity, especially the type I and III interferon (IFN) production, contributes to the pathogenesis of COVID-19. However, how SARS-CoV-2 evades antiviral immunity still needs further investigations. Here, we reported that the open reading frame 9b (ORF9b) protein encoded by the SARS-CoV-2 genome inhibits the activation of type I and III IFN response by targeting multiple molecules of innate antiviral signaling pathways. SARS-CoV-2 ORF9b impaired the induction of type I and III IFNs by Sendai virus or the dsRNA mimic poly (I:C). SARS-CoV-2 ORF9b inhibits the activation of type I and III IFNs induced by the components of cytosolic dsRNA-sensing pathways of RIG-I/MDA5-MAVS signaling, including RIG-I, MDA-5, MAVS, TBK1, and IKK{varepsilon} rather than IRF3-5D, the active form of IRF3. SARS-CoV-2 ORF9b also suppressed the induction of type I and III IFNs by TRIF and STING, the adaptor protein of endosome RNA-sensing pathway of TLR3-TRIF signaling and the adaptor protein of cytosolic DNA-sensing pathway of cGAS-STING signaling, respectively. Mechanistically, SARS-CoV-2 ORF9b protein interacts with RIG-I, MDA-5, MAVS, TRIF, STING, TBK1, and prevents TBK1 phosphorylation, thus impeding the phosphorylation and nuclear trans-localization of IRF3 activation. Overexpression of SARS-CoV-2 ORF9b facilitates the replication of the vesicular stomatitis virus. Therefore, SARS-CoV-2 ORF9b negatively regulates antiviral immunity, thus, facilitate virus replication. This study contributes to our understanding of the molecular mechanism of how SARS-CoV-2 impaired antiviral immunity and providing an essential clue to the pathogenesis of COVID-19.

A Systemic and Molecular Study of Subcellular Localization of SARS-CoV-2 Proteins (preprint)

Coronavirus possesses the largest RNA genome among all the RNA viruses. Its genome encodes about 29 proteins. Most of the viral proteins are non-structural proteins (NSP) except envelop (E), membrane (M), nucleocapsid (N) and Spike (S) proteins that constitute the viral nucleocapsid, envelop and surface. We have recently cloned all the 29 SARS-CoV-2 genes into vectors for their expressions in mammalian cells except NSP11 that has only 14 amino acids (aa). We are able to express all the 28 cloned SARS-CoV-2 genes in human cells to characterize their subcellular distributions. The proteins of SARS-CoV-2 are mostly cytoplasmic but some are both cytoplasmic and nuclear. Those punctate staining proteins were further investigated by immunofluorescent assay (IFA) using specific antibodies or by co-transfection with an organelle marker-expressing plasmid. As a result, we found that NSP15, ORF6, M and ORF7a are related to Golgi apparatus, and that ORF7b, ORF8 and ORF10 colocalize with endoplasmic reticulum (ER). Interestingly, ORF3a distributes in cell membrane, early endosome, endosome, late endosome and lysosome, which suggests that ORF3a might help the infected virus to usurp endosome and lysosome for viral use. Furthermore, we revealed that NSP13 colocalized with SC35, a protein standing for splicing compartments in the nucleus. Our studies for the first time visualized the subcellular locations of SARS-CoV-2 proteins and might provide novel insights into the viral proteins biological functions.

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Membrane (M) Protein Inhibits Type I and III Interferon Production by Targeting RIG-I/MDA-5 Signaling (preprint)

The coronavirus disease 2019 (COVID-19) caused by Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has quickly spread worldwide and has infected more than ten million individuals. One of the typical features of COVID-19 is that both type I and III interferon (IFN)-mediated antiviral immunity are suppressed. However, the molecular mechanism by which SARS-CoV-2 evades this antiviral immunity remains elusive. Here, we report that the SARS-CoV-2 membrane (M) protein inhibits the production of type I and III IFNs induced by the cytosolic dsRNA-sensing pathway of RIG-I/MDA-5-MAVS signaling. The SARS-CoV2 M protein also dampens type I and III IFN induction stimulated by Sendai virus infection or poly (I:C) transfection. Mechanistically, the SARS-CoV-2 M protein interacts with RIG-I, MAVS, and TBK1 and prevents the formation of a multi-protein complex containing RIG-I, MAVS, TRAF3, and TBK1, thus impeding IRF3 phosphorylation, nuclear translocation, and activation. Consequently, the ectopic expression of the SARS-CoV2 M protein facilitates the replication of vesicular stomatitis virus (VSV). Taken together, the SARS-CoV-2 M protein antagonizes type I and III IFN production by targeting RIG-I/MDA-5 signaling, which subsequently attenuates antiviral immunity and enhances viral replication. This study provides insight into the interpretation of the SARS-CoV-2-induced antiviral immune suppression and sheds light on the pathogenic mechanism of COVID-19.