Viral load dynamics and disease severity in patients infected with SARS-CoV-2 in Zhejiang province, China, January-March 2020: retrospective cohort study

Zheng, Shufa; Fan, Jian Gao; Yu, Fei; Feng, Baihuan; Liu, Bin; Zou, Qianda; Xie, Guoliang; Lin, Sha; Wang, Ruonan; Yang, Xianzhi; Chen, Weizhen; Wang, Qi; Zhang, Dan Feng; Liu, Yanchao; Gong, Rui; Ma, Zhaohui; Lu, Shu‐Ling; Xiao, Yanyan; Gu, Yaxi; Zhang, Jinming; Yao, Hang‐Ping; Xu, Kaijin; Lu, Xin-Jiang; Wei, Guoqing; Zhou, Jianying; Fang, Qiang; Cai, Hongliu; Qiu, Yunqing; Sheng, Jifang; Chen, Yu; Liang, Tingbo

doi:10.1136/bmj.m1443

Cited by 1,401 publications

(1,714 citation statements)

References 32 publications

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“…3 In one study, PCR positivity in stool was observed in 55 of 96 (57%) infected patients and remained positive in stool beyond nasopharyngeal swab by a median of 4 to 11 days, but was unrelated to clinical severity. 2 Persistence of PCR in sputum and stool was found to be similar as assessed by Wölfel et al 3 In a study of 205 patients with confirmed COVID-19 infection, RT-PCR positivity was highest in bronchoalveolar lavage specimens (93%), followed by sputum (72%), nasal swab (63%), and pharyngeal swab (32%). 5 False-negative results mainly occurred due to inappropriate timing of sample collection in relation to illness onset and deficiency in sampling technique, especially of nasopharyngeal swabs.…”

supporting

confidence: 65%

Interpreting Diagnostic Tests for SARS-CoV-2

Sethuraman

Jeremiah

Ryo

2020

JAMA

1,437

1,509

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supporting

confidence: 65%

Interpreting Diagnostic Tests for SARS-CoV-2

Sethuraman

Jeremiah

Ryo

2020

JAMA

1,437

1,509

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“…Viral load dynamics and disease severity were reported by Zheng et al [14]. From 96 consecutive patients, RNA viral load was measured in respiratory, stool, serum and urine samples (total number of samples 3497).…”

Section: Viremia and Viral Loadmentioning

confidence: 94%

COVID-19 update: Covid-19-associated coagulopathy

Becker

2020

J Thromb Thrombolysis

614

646

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We are too much accustomed to attribute to a single cause that which is the product of several, and the majority of our controversies come from that. Marcus AureliusThe Covid-19 pandemic has introduced an array of organspecific and systemic phenotypes-some previously observed in viral infections, including severe acute respiratory syndrome (SARS) and others that appear to be unique to SARScoronavirus (CoV)-2. Rapidly emerging information from clinical observations, autopsy-based findings, extrapolations from in vitro and ex vivo studies and dynamic modeling are informing management guidelines; however, many questions remain unanswered and clinical trials that are required to provide evidence have not been completed in most areas. Among the many questions that require careful thought, reflection and investigation are the mechanism(s) underlying the development of a systemic coagulopathy and acquired thrombophilia characterized in a majority of cases by a proclivity for venous, arterial and microvascular thrombosis.The following review summarizes emerging insights into the pathobiology, mechanism(s), diagnosis, management, foundations for research and either planned or ongoing clinical trials for Covid-19-associated coagulopathy.

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“…severity of SARS-CoV-2 infection (Zheng et al, 2020). The time to reach a detectable viral load depends on the growth rate of the viral population, which is to the leading order…”

Section: Time To Detectable Viral Loadmentioning

confidence: 99%

Predicted success of prophylactic antiviral therapy to block or delay SARS-CoV-2 infection depends on the drug’s mechanism of action

Czuppon

Débarre

Gonçalves

et al. 2020

Preprint

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Repurposed drugs that are immediately available and have a good safety profile constitute a first line of defense against new viral infections. Despite a limited antiviral activity against SARS-CoV-2, several drugs serve as candidates for application, not only in infected individuals but also as prophylaxis to prevent infection establishment. Here we use a stochastic model to describe the early phase of a viral infection. We find that the critical efficacy needed to block viral establishment is typically above 80%. This value can be improved by combination therapy. Below the critical efficacy, establishment can still sometimes be prevented; for that purpose, drugs blocking viral entry into target cells (or equivalently enhancing viral clearance) are more effective than drugs reducing viral production or enhancing infected cell death. When a viral infection cannot be prevented because of high exposure or low drug efficacy, antivirals can still delay the time to reach detectable viral loads from 4 days when untreated to up to 30 days. This delay flattens the within-host viral dynamic curve, and possibly reduces transmission and symptom severity. These results suggest that antiviral prophylaxis, even with reduced efficacy, could be efficiently used to prevent or alleviate infection in people at high risk. It could thus be an important component of the strategy to combat the SARS-CoV-2 pandemic in the months or years to come.

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Viral load dynamics and disease severity in patients infected with SARS-CoV-2 in Zhejiang province, China, January-March 2020: retrospective cohort study

Cited by 1,401 publications

References 32 publications

Interpreting Diagnostic Tests for SARS-CoV-2

Interpreting Diagnostic Tests for SARS-CoV-2

COVID-19 update: Covid-19-associated coagulopathy

Predicted success of prophylactic antiviral therapy to block or delay SARS-CoV-2 infection depends on the drug’s mechanism of action

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