Summary Knowledge of the incubation period is essential in the investigation and control of infectious disease, but statements of incubation period are often poorly referenced, inconsistent, or based on limited data. In a systematic review of the literature on nine respiratory viral infections of public-health importance, we identified 436 articles with statements of incubation period and 38 with data for pooled analysis. We fitted a log-normal distribution to pooled data and found the median incubation period to be 5·6 days (95% CI 4·8–6·3) for adenovirus, 3·2 days (95% CI 2·8–3·7) for human coronavirus, 4·0 days (95% CI 3·6–4·4) for severe acute respiratory syndrome coronavirus, 1·4 days (95% CI 1·3–1·5) for influenza A, 0·6 days (95% CI 0·5–0·6) for influenza B, 12·5 days (95% CI 11·8–13·3) for measles, 2·6 days (95% CI 2·1–3·1) for parainfluenza, 4·4 days (95% CI 3·9–4·9) for respiratory syncytial virus, and 1·9 days (95% CI 1·4–2·4) for rhinovirus. When using the incubation period, it is important to consider its full distribution: the right tail for quarantine policy, the central regions for likely times and sources of infection, and the full distribution for models used in pandemic planning. Our estimates combine published data to give the detail necessary for these and other applications.

https://www.thelancet.com/pdfs/journals/laninf/PIIS1473-3099(09)70069-6.pdf

Incubation periods of acute respiratory viral infections: a systematic review

To identify immunological predictors of resistance to influenza A infection and illness, the immunological status of live and inactivated virus vaccines subsequently challenged with H1N1 or H3N2 wild-type virus was examined. We refer to prechallenge antibodies of vaccinees receiving live attenuated virus as infection induced and those receiving inactivated virus as inactivated vaccine induced. Inactivated vaccine-induced protection against wild-type virus infection or illness correlated with the level of neuraminidase-inhibiting antibody in serum, local hemagglutinin immunoglobulin G (IgG) (but not IgA) enzyme-linked immunosorbent assay antibody, and hemagglutination-inhibiting antibody in serum. In contrast, infection-induced resistance to wild-type virus infection correlated with local hemagglutinin IgA antibody and neuraminidase-inhibiting antibody in serum, but not with hemagglutination-inhibiting antibody in serum. These observations suggest that live vaccine virus infection-induced and inactivated vaccine-induced immunity may involve different compartments of the immune system; sufficient antibody in either serum or nasal secretions is capable of conferring resistance.

https://jcm.asm.org/content/jcm/24/1/157.full.pdf

Serum and nasal wash antibodies associated with resistance to experimental challenge with influenza A wild-type virus.

Influenza A viruses (IAVs) cause epidemics and pandemics that result in considerable financial burden and loss of human life. To manage annual IAV epidemics and prepare for future pandemics, an improved understanding of how IAVs emerge, transmit, cause disease and acquire pandemic potential is urgently needed. Fundamental techniques essential for procuring such knowledge are IAV isolation and culture from experimental and surveillance samples. Here we present a detailed protocol for IAV sample collection and processing, amplification in chicken eggs or mammalian cells, and identification from samples containing unknown pathogens. This protocol is robust, and it allows for the generation of virus cultures that can be used for downstream analyses. Once experimental or surveillance samples are obtained, virus cultures can be generated and the presence of IAVs can be verified in 3-5 d via reverse-transcription (RT)-PCR or hemagglutination assay. Increased time frames may be required for less experienced laboratory personnel, or when large numbers of samples will be processed.

/pdf/influenza-a-virus-isolation-culture-and-identification-46nqbgxtw6.pdf

Influenza A virus isolation, culture and identification

/pdf/serum-proteins-and-antibody-activity-in-human-nasal-55sq3bs8kb.pdf

Serum Proteins and Antibody Activity in Human Nasal Secretions

Dogs, of all domestic animals, are the most common source of human rabies. 1 In the United States, 600,000 to 1,000,000 people are bitten by dogs each year. 2 Of the 212 human deaths from rabies from 1946 to 1959, where the species of biting animal was known, 84% were attributed to dogs. 1 The total number of reported human deaths due to rabies in this period markedly decreased. 3 Because the United States' population of dogs increased from about 12 million in 1946 1 to approximately 25 million in 1960, 4 and is possibly still increasing, it is reasonable to expect that in the next decade many more physicians will have to decide whether or not to administer antirabies treatment to a person who has been bitten by a dog. As part of this decision the physician will have to consider carefully the evidence for true exposure to rabies

https://jamanetwork.com/journals/jama/articlepdf/656160/jama_193_5_010.pdf

Excretion of Street Rabies Virus in the Saliva of Dogs

Rabies vaccine encephalomyelitis in relation to the incidence of animal rabies in Los Angeles.

The Effect of Subcutaneous Vaccination with Influenza Virus upon the Virus.Inactivating Capacity of Nasal Secretions.

Studies of the distribution of poliomyelitis virusi. in the environment of sporadic cases

Studies of the distribution of poliomyelitis virusii. in a small town

Immunity in Human Subjects Artificially Infected with Influenza Virus, Type B.

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