Like I said. This isn't the 2003 SARS pandemic.
Rejection of the findings regrading asymptomatic/presymptomatic transmission on the basis of SARS-CoV-1 characteristics is essentially baseless. You continued to say there was no documented evidence, even when shown that there clearly was.
None of the studies into asymptomatic (or "presymptomatic") transmission are including cases which haven't been confirmed as SARS-COV-2 by PCR, and the
possibilities for methods of transmission excluding coughing or sneezing have been adequately established even if they have yet to be accurately attributed statistically at this stage.
The precedent of SARS-CoV-1 characteristics have driven and guided the research of SARS-CoV-2 since it was discovered, it may have been a hint that one is called SARS-CoV-1 and the other is called SARS-CoV-2, this is because after the discovery of the nCoV2019 they classified it as being in the subgenera
Sarbecovirus due to genetic similarity to SAR-CoV(1), thus SAR-CoV-2
https://www.nature.com/articles/s41564-020-0695-z#Fig2
initial studies demonstrated "2019-nCoV caused clusters of fatal pneumonia with clinical presentation
greatly resembling SARS-CoV."
https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(20)30183-5/fulltext
So, in the beginning " The initial working case definitions for suspected NCIP {Novel Coronavirus–Infected Pneumonia} were based on the SARS and Middle East respiratory syndrome (MERS) case definitions, as recommended by the World Health Organization (WHO) in 2003 and 2012 " with a consideration for a connection to the seafood market, until January 18th when they began performing specific tests
"We estimated an R0 of approximately 2.2 {for SARS-CoV-1} , meaning that on average each patient has been spreading infection to 2.2 other people. In general, an epidemic will increase as long as R0 is greater than 1, and control measures aim to reduce the reproductive number to less than 1. The R0 of SARS was estimated to be around 3"
"Although infections in health care workers have been detected {for SARS-CoV-1}, the proportion has not been as high as during the SARS and MERS outbreaks."
"Super-spreading events have not yet been identified for NCIP, but they could become a feature as the epidemic progresses."
https://www.nejm.org/doi/10.1056/NEJMoa2001316
"It appears that 2019-nCoV uses the same cellular receptor as SARS-CoV (human angiotensin-converting enzyme 2 [hACE2]),
3 so transmission is expected only after signs of lower respiratory tract disease develop. SARS-CoV mutated over the 2002–2004 epidemic to better bind to its cellular receptor and to optimize replication in human cells, enhancing virulence.
7 Adaptation readily occurs because coronaviruses have error-prone RNA-dependent RNA polymerases, making mutations and recombination events frequent. By contrast, MERS-CoV has not mutated substantially to enhance human infectivity since it was detected in 2012."
{based on the shared characteristics of SARS-CoV 1&2 (hACE2 receptor transmission) SARS-CoV-2 doesn't begin transmission until you get symptoms which is of course logical as the viral load is highest after onset of symptoms}
https://www.nejm.org/doi/full/10.1056/NEJMe2001126
"Together, these observations suggest that the affinity of S protein for ACE2 is an important determinant in the overall rate of viral replication and in the severity of disease. If so, adaptations within the S protein that are critical for high‐affinity association with human ACE2 may have contributed to the unusual severity of SARS."
{hACE2 receptor strong determinant for overall rate of viral replication and in the severity of disease}
https://www.embopress.org/doi/10.1038/sj.emboj.7600640
"In addition, we found bat SARSr-CoV strains with different S proteins that can all use the receptor of SARS-CoV in humans (ACE2) for cell entry, suggesting diverse SARSr-CoVs capable of direct transmission to humans are circulating in bats in this cave. Our current study therefore offers a clearer picture on the evolutionary origin of SARS-CoV and highlights the risk of future emergence of SARS-like diseases."
{from 2017, eerily predictive}
https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1006698
"Currently, there was no evidence of air-borne transmission. Viral RNAs could be found in nasal discharge, sputum, and sometimes blood or feces.1,9,10,13,15 But whether oral-fecal transmission can happen has not yet been confirmed. Once people are infected by the 2019-nCoV, it is believed that, like SARS,
there is no infectivity until the onset of symptoms.15
However, one report describes infection from an asymptomatic contact but the investigation was not solid.10 The infectious doses for 2019-nCoV is not clear, but a high viral load of up to 108 copies/mL in patient’s sputum has been reported.10 The viral load increases initially and still can be detected 12 days after onset of symptoms.9 Therefore, the infectivity of patients with 2019-nCoV may last for about 2 weeks. However, whether infectious viral particles from patients do exist at the later stage requires validation."
{wow crazy how these guys came to same conclusion as me from logical analysis, your mind must be blown lol}
https://journals.lww.com/jcma/FullText/2020/03000/The_outbreak_of_COVID_19__An_overview.3.aspx