Fitting a mechanistic model to data from SARS-CoV-2 source-recipient pairs generates improved estimates of changes in infectiousness during infection, indicating substantial transmission shortly before symptom onset.
Broader case variation in respiratory viral load, and in shedding virus via droplets and aerosols, for SARS-CoV-2 than influenza A(H1N1)pdm09 facilitates greater transmission heterogeneity in the COVID-19 pandemic than the 2009 flu pandemic.
Virus infection of the central nervous system disrupts the homeostasis of the immune-neural-synaptic axis via induction of pleiotropic genes with an unintended off-target negative impact on the neurotransmission.
In mouse models of Huntington's disease, the subthalamic nucleus, which suppresses movements, also exhibits impaired glutamate homeostasis, NMDA receptor-dependent mitochondrial oxidant stress, firing disruption, and 30% neuronal loss.
The increased risk for symptomatic malaria following an asymptomatic Plasmodium falciparum infection supports targeting asymptomatic infections as a tool to reduce clinical malaria in high-transmission settings.
3% of >1,000 asymptomatic healthcare workers in their workplace tested positive for SARS-CoV-2, suggesting that comprehensive screening programmes are vital to prevent acquisition of COVID-19 in hospitals.