![]() If patient A is the index patient, infected in Wuhan, her incubation period would have been 28 days, which would be extremely long, according to updated information (W.J. Despite symptom resolution, on January 30 she was confirmed to have SARS-CoV-2 infection. On January 15–16, 2020, she had a fever, but symptoms resolved without treatment. ![]() Patient A, a 30-year-old woman, the only case-patient who indicated that she had been in Wuhan, China, returned from Wuhan on December 18, 2019. The Wenzhou Center for Disease Control and Prevention traced and tested their contacts, and by January 28, COVID-19 was confirmed for 7 persons (patients A–G) from the same office (on floor 7). On January 21, COVID-19 was confirmed for patient E and his co-worker, patient G. On January 20, 2020, a 23-year-old man (patient E) sought care at a hospital after 11 days of fever and headache. The study was approved with written consent from the Ethics Committee of Wenzhou Central Hospital and written informed consent from all case-patients. We analyzed clinical and laboratory data for cases by using real-time reverse transcription PCR ( 1). To determine how the virus may have spread among a cluster of COVID-19 cases associated with a shopping mall in Wenzhou (a city with 8 million residents), China, we monitored and traced close contacts and hypothesized possible transmission modes. However, these transmission modes do not explain all cases. Elucidation of the factors related to the genesis of the strong inflammatory response occurring early during the infectious process in these asymptomatic individuals could increase our understanding of the disease.Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease (COVID-19), is presumed to spread primarily via respiratory droplets and close contact. ![]() The lack of genetic differences between symptomatic and asymptomatic individuals suggest that asymptomatic Ebola infection did not result from viral mutations. This study showed that asymptomatic, replicative Ebola infection can and does occur in human beings. Asymptomatic individuals had a strong inflammatory response characterised by high circulating concentrations of cytokines and chemokines. The glycoprotein and viral protein of 24 kDa genes showed no nucleotide differences between symptomatic and asymptomatic individuals. Western-blot analysis showed that IgG responses were directed to nucleoprotein and viral protein of 40 kDa. PCR products were then sequenced.ġ1 of 24 asymptomatic individuals developed both IgM and IgG responses to Ebola antigens, indicating viral infection. ![]() RNA was extracted from peripheral blood mononuclear cells, and reverse transcriptase-PCR assays were done to amplify RNA of Ebola virus. Serum samples were analysed for the presence of Ebola antigens, virus-specific IgM and IgG (by ELISA and western blot), and different cytokines and chemokines. These asymptomatic individuals were sampled 2, 3, or 4 times during a 1-month period after the first exposure to symptomatic patients. We aimed to determine whether these individuals were indeed infected with Ebola virus, and how they maintained asymptomatic status.īlood was collected from 24 close contacts of symptomatic patients. During both outbreaks we identified some individuals in direct contact with sick patients who never developed symptoms. Two outbreaks of fulminating haemorrhagic fever occurred in northern Gabon in 1996, with a 70% case-fatality rate. Ebola virus is one of the most virulent pathogens, killing a very high proportion of patients within 5-7 days. ![]()
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