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Viral infection is the invasion of the body by a small agent known as a virus. Viruses replicate inside host cells and can produce toxins that cause disease. The immune system helps to destroy viruses, but antiviral immune responses can also cause tissue damage and illness.
SARS-CoV-2 infection can be associated with ‘brain fog’ and persistent neurologic disease, especially in the elderly, with the possibility of direct viral particle interference with normal synaptic transmission.
Profiling of plasma proteins in individuals with COVID-19 shows that complement activation and myeloid inflammation are major pathways in the pathogenesis of long COVID and identifies distinct profiles of immune dysregulation in individuals with long COVID, highlighting the heterogeneous and diverse nature of this disease.
Immunization via the respiratory route is predicted to increase the effectiveness of SARS-CoV-2 vaccines. Here, Kaiser et al. describe a murine pneumonia virus vectored vaccine expressing spike protein, and show that intranasal immunization of male rhesus macaques provides good mucosal and systemic immunogenicity and efficacy.
In this study, the authors report that bat H9N2 influenza A virus replicates and transmits in ferrets, efficiently infects human lung explant cultures, evades MxA antiviral activity in mice, and has low antigenic similarity to seasonal N2, meeting pre-pandemic criteria.
Knowledge of pathogenesis mechanisms and effective treatments for viral myocarditis is lacking. Here, Wang et al show that loss of TRIM29 and PERK inhibitor mitigate viral myocarditis by attenuating PERK-driven ER stress and ROS responses in male mice.
The chemokine receptors CCR2 and CCR7 synergistically regulate recruitment of inflammatory monocytes from the bone marrow to the brain of mice infected with La Crosse and Herpes Simplex virus.
SARS-CoV-2 infection can be associated with ‘brain fog’ and persistent neurologic disease, especially in the elderly, with the possibility of direct viral particle interference with normal synaptic transmission.
Profiling of plasma proteins in individuals with COVID-19 shows that complement activation and myeloid inflammation are major pathways in the pathogenesis of long COVID and identifies distinct profiles of immune dysregulation in individuals with long COVID, highlighting the heterogeneous and diverse nature of this disease.
The implementation of PCR tests of pooled saliva samples for universal screening of congenital cytomegalovirus infection was assessed in 15,805 neonates over 13 months. This extensive analysis revealed the high feasibility and empirical efficiency of the pooled testing approach, which had a clinically insignificant loss of sensitivity.
T cell- and antibody-based immunological protection are generally considered to function together, but data now show how T cells conferred by previous SARS-CoV-2 infection or two-dose vaccination can elicit heterologous protection in mice against subsequent SARS-CoV-2 infection, even in the absence of antibodies.
Drivers of persistent symptoms after acute COVID-19 remain largely unknown. Alterations in immune function, iron homeostasis and dysregulated erythropoiesis are described as treatable correlates of post-acute sequelae of COVID-19.