Background. Since December 2019, SARS-CoV-2 has extended to most parts of China with >80 000 cases and to at least 100 countries with >60 000 international cases as of 15 March 2020. Here we used a household cohort study to determine the features of household transmission of COVID-19.Methods. A total of 105 index patients and 392 household contacts were enrolled. Both index patients and household members were tested by SARS-CoV-2 RT-PCR. Information on all recruited individuals was extracted from medical records and confirmed or supplemented by telephone interviews. The baseline characteristics of index cases and contact patients were described. Secondary attack rates of SARS-CoV-2 to contact members were computed and the risk factors for transmission within the household were estimated.Results. Secondary transmission of SARS-CoV-2 developed in 64 of 392 household contacts (16.3%). The secondary attack rate to children was 4% compared with 17.1% for adults. The secondary attack rate to the contacts within the households with index patients quarantined by themselves since onset of symptoms was 0% compared with 16.9% for contacts without quarantined index patients. The secondary attack rate to contacts who were spouses of index cases was 27.8% compared with 17.3% for other adult members in the households.Conclusions. The secondary attack rate of SARS-CoV-2 in household is 16.3%. Age of household contacts and spousal relationship to the index case are risk factors for transmission of SARS-CoV-2 within a household. Quarantine of index patients at home since onset of symptoms is useful to prevent the transmission of SARS-Co-2 within a household.
Angiotensin converting enzyme 2 (ACE2) is a lately discovered enzyme catalyzing Angiotensin II into Angiotensin (1-7). Angiotensin II has been reported to impair endothelial progenitor cell (EPC) function and is detrimental to stroke. Here, we studied the role of ACE2 in regulating EPC function in vitro and in vivo. EPCs were cultured from human renin and angiotensinogen transgenic (R+A+) mice and their controls (R-A-). In in vitro experiments, EPCs were transduced with lentivirus-ACE2 (Lenti-ACE2) or Lenti-GFP. The effects of ACE2 over-expression on EPC function and endothelial oxide synthase (eNOS)/NADPH oxidase (Nox) expression were determined. ACE2, eNOS and Nox inhibitors were used for pathway validation. In in vivo studies, the therapeutic efficacy of EPCs over-expressing ACE2 was determined at day 7 after ischemic stroke induced by middle cerebral artery occlusion. We found that 1) Lenti-ACE2 transduction resulted in a four-fold increase of ACE2 expression in EPCs. This was accompanied with an increase in eNOS expression and nitric oxide production, and a decrease in Nox2, 4 expression and reactive oxygen species production. 2) ACE2 over-expression improved the abilities of EPC migration and tube formation which were impaired in R+A+ mice. These effects were inhibited by ACE2 or eNOS inhibitor and further enhanced by Nox inhibitor. 3) Transfusion of Lenti-ACE2 primed EPCs reduced cerebral infarct volume and neurologic deficits, increased cerebral microvascular density and angiogenesis. Our data demonstrate that ACE2 improves EPC function via regulating eNOS and Nox pathways and enhances the efficacy of EPC-based therapy for ischemic stroke.
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