Most probably from bats via intermediate animal hosts to index case.47 104

All subsequent cases resulted from human-to-human transmission.

Mainly through respiratory droplets from infected persons105; by hands, after contamination at nose, mouth or eyes; also through air on exposure to sneezing or coughing from an infected person at close distance.

Through aerosols, while singing/talking loudly in congregations, groups, parties, karaoke, and so on, especially in poorly ventilated spaces.18 106

Through fomites.107

Possibly via faecal–oral route108 109; detection in sewage.110–112

Related to peak in upper respiratory tract viral load prior to symptom onset in presymptomatic (paucisymptomatic) persons.106 113 114

Transmission dynamics in asymptomatic persons not fully elucidated although viral shedding occurs.115

Influence of climate on the capacity of the virus to survive outside human body (in air, in droplets, on surfaces, etc.) and to spread has been speculative.

May spread more readily in milder/colder climate116 117; although variability of the reproductive number could not be explained by temperature or humidity.118

Existing levels of air pollution may play a role; air pollutants, such as particulate matter, nitrogen dioxide and carbon monoxide, are likely a factor facilitating longevity of virus particles.119

Elevated exposure to common particulate matter can alter host immunity to respiratory viral infections.119

IgM and IgA antibody response 5–10 days after onset of symptoms, does not depend on clinical severity, correlates with virus neutralisation; IgG is observed ~14 days after onset of symptoms,93 120 may or may not correspond to protective immunity. Whether antibody response is long lasting has remained unclear.

Rechallenge in rhesus macaques showed immunity post primary infection.121 How protective immunity after first infection is against subsequent infection with an identical or mutated strain has been uncertain.

Incidental reports showed recovered persons positive by real-time PCR,122 123 later attributed to testing errors.

Reported estimates for seroprevalence range between 0.4% and 59.3%124; differences in timing of the serosurvey, the use of assay kits with varying sensitivity/specificity, and different methods for detection may contribute to this large variation.125

Seemingly high seroprevalence may be due to cross-reactive epitopes between SARS-CoV-2 and other HCoVs.126 127

Whether seroprevalence implies immune protection is unclear, yet, some countries have considered use of ‘immunity passports’.128

For herd immunity to be effectively achieved, an estimated seroprevalence of 60% of the population will be required.37 Other studies estimate between 5.66% and 85% seroprevalence in different countries.129–131

Mutation rate: ~10⁻³ substitutions per year per site132 133; 13 mutation sites have been identified as of May 2020, suggesting selective mutations.134

The low mutation rate suggests that a vaccine would be a single vaccine rather than a new vaccine every year like the influenza vaccine.135

Ten different circulating clades (nextstrain.org; www.gisaid.org),136 as of May 2020.