No abstract

We report temporal patterns of viral shedding in 94 laboratory-confirmed COVID-19 patients and modelled COVID-19 infectiousness profile from a separate sample of 77 infector-infectee transmission pairs. We observed the highest viral load in throat swabs at the time of symptom onset, and inferred that infectiousness peaked on or before symptom onset. We estimated that 44% of transmission could occur before first symptoms of the index. Disease control measures should be adjusted to account for probable substantial pre-symptomatic transmission.

The novel coronavirus (2019-nCoV) infection caused pneumonia. we retrospectively analyzed the virus presence in the pharyngeal swab, blood, and the anal swab detected by real-time PCR in the clinical lab. Unexpectedly, the 2109-nCoV RNA was readily detected in the blood (6 of 57 patients) and the anal swabs (11 of 28 patients). Importantly, all of the 6 patients with detectable viral RNA in the blood cohort progressed to severe symptom stage, indicating a strong correlation of serum viral RNA with the disease severity (p-value = 0.0001). Meanwhile, 8 of the 11 patients with annal swab virus-positive was in severe clinical stage. However, the concentration of viral RNA in the anal swab (Ct value = 24 + 39) was higher than in the blood (Ct value = 34 + 39) from patient 2, suggesting that the virus might replicate in the digestive tract. Altogether, our results confirmed the presence of virus RNA in extra-pulmonary sites. ARTICLE HISTORY

Eukaryotic cells have evolved extensive protein quality-control mechanisms to remove faulty translation products. Here, we show that yeast cells continually produce faulty mitochondrial polypeptides that stall on the ribosome during translation but are imported into the mitochondria. The cytosolic protein Vms1, together with the E3 ligase Ltn1, protects against the mitochondrial toxicity of these proteins and maintains cell viability under respiratory conditions. In the absence of these factors, stalled polypeptides aggregate after import and sequester critical mitochondrial chaperone and translation machinery. Aggregation depends on C-terminal alanyl/threonyl sequences (CAT-tails) that are attached to stalled polypeptides on 60S ribosomes by Rqc2. Vms1 binds to 60S ribosomes at the mitochondrial surface and antagonizes Rqc2, thereby facilitating import, impeding aggregation, and directing aberrant polypeptides to intra-mitochondrial quality control. Vms1 is a key component of a rescue pathway for ribosome-stalled mitochondrial polypeptides that are inaccessible to ubiquitylation due to coupling of translation and translocation.

and colleagues at ETH Zurich very helpfully alerted us to a syntactical error in our original code, specifically that the likelihood as we had originally specified gave rise to zero probability for two transmission pairs with the most negative serial intervals. Following their lead, we also applied a normalization factor in the likelihood to account for the uncertainty in the symptom-onset dates of the index cases. However, assuming a uniform distribution, the likelihood would differ only by a multiplicative constant and would give the same estimates. We used the bootstrap method to estimate the 95% confidence intervals (CIs).

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No abstract

In recent decades, the impact of dengue has increased both geographically and in intensity, and this disease is now a threat to approximately half of the world's population. An unexpected large outbreak of dengue fever was reported in Xishuangbanna Dai Autonomous Prefecture, Yunnan Province, China, in 2013. This was the first autochthonous outbreak with a significant proportion of severe dengue cases in mainland China in a decade. According to the 2009 World Health Organization guidelines, half of the 136 laboratory confirmed cases during the epidemic were severe dengue. The clinical presentation included severe haemorrhage (such as massive vaginal and gastrointestinal bleeding), severe plasma leakage (such as pleural effusion, ascites, or hypoproteinaemia), and organ involvement (such as myocarditis and lung impairment); 21 cases eventually deteriorated to shock. During this outbreak, all severe cases occurred in adults, among whom about 43% had co-morbid conditions. Nucleic acid detection and virus isolation confirmed dengue virus serotype 3 (DENV-3) to be the pathogenic agent of this outbreak. Phylogenetic analyses of envelope gene sequences showed that these DENV-3 isolates belonged to genotype II. This finding is of great importance to understand the circulation of DENV and predict the risk of severe disease in mainland China. Here, we provide a brief report of the epidemiology, clinical manifestations, and aetiology of this dengue fever outbreak, and characterize DENV strains isolated from clinical specimens.