Aerosolization at low humidity inactivates encephalomyocarditis virus by damaging its protein coat, though the viral RNA remains infectious.
May inform humidity-based strategies to limit aerosol virus viability in clinical settings; leaves open translation from animal models to human pathogens.
After aerosolization at relative humidities of 50% or lower, encephalomyocarditis virus is rapidly inactivated. In this process the protein coat of the virion is damaged. This appears as a loss of hemagglutination activity and loss of affinity for hemagglutination inhibiting antibodies. The ribonucleic acid of the virus retains its infectivity but it becomes susceptible to ribonuclease. It sediments in sucrose gradients when centrifuged at high speed with the same velocity as free infectious ribonucleic acid extracted with phenol from intact encephalomyocarditis virus.
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Jong et al. (1974) studied this question.
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