Please read Dr. Cristea’s article in the Journal of Allergy and Clinical Immunology titled, “Intercellular communication within the virus microenvironment affects the susceptibility of cells to secondary viral infections.“
Cell-to-cell communication is the basis of multicellular life, response to environmental cues, and development of disease. The remarkable capacity of viruses to manipulate host intracellular processes is essential for establishing an infection, but less is understood about how viruses control intercellular communication and how this affects the spread of infection in tissue. Primary infection of a cell or reactivation from viral latency establishes a localized virus microenvironment (VME). In a VME, cell nonautonomous signaling pathways must be reprogrammed by either the virus or the host to promote or suppress viral spread, respectively. From the perspective of the host, intracellular sensing of pathogen-associated molecular patterns derived from the virus leads to activation of intrinsic and innate immune responses to induce the secretion of type I interferons (IFNs), other cytokines, and chemokines. Receptor-mediated recognition of these signaling molecules by uninfected cells adjacent to the infection site induces the expression of IFN-stimulated genes (ISGs), which restrict intrinsic viral entry and replication. Innate and adaptive immune cells, including natural killer cells, B cells, and T cells, are further recruited to clear the infection in vivo. However, in a VME, infection-adjacent cells that receive transduced messages may concomitantly undergo proviral alterations to promote virus spread. To read the full article.
Intercellular communication within the virus microenvironment affects the susceptibility of cells to secondary viral infections. Song B, Sheng X, Justice JL, Lum KK, Metzger PJ, Cook KC, Kostas JC, Cristea IM. Sci Adv. 2023 May 10;9(19):eadg3433. PMID: 37163594 PMCID: PMC10171814 DOI: 10.1126/sciadv.adg3433