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Alphavirus Neurovirulence
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Katherine Taylor, Slobodan Paessler
The second phase of the immune response to alphavirus infection is characterized by the waning of type I IFN and the development of a robust cell-mediated immunity that theoretically limits CNS damage and clears the virus from circulation and sites of replication.
Understanding host responses to equine encephalitis virus infection: implications for therapeutic development
Published in Expert Review of Anti-infective Therapy, 2022
Kylene Kehn-Hall, Steven B. Bradfute
Global analysis of the transcriptome following alphavirus infection has identified multiple cellular pathways that are altered upon infection and also shed light on specific cellular factors that are utilized for more efficient viral replication. As mentioned above, there have been multiple transcriptomic studies that identified upregulation of proinflammatory cytokines and chemokines, as well as immune response factors, such as TLRs in the brains of mice infected with virulent VEEV [26,31,53,54]. Likewise, a transcriptomics study on brain samples from C3H/Ne mice infected intranasally with VEEV TC-83 found significant alterations in immune and inflammatory response pathways, including gene expression changes of factors involved in signaling between natural killer (NK) cells and antigen presenting cells [116]. These changes led the authors to deplete NK cells, which protected the C3H/Ne mice from VEEV-induced mortality. NHPs exposed to aerosolized VEEV also displayed upregulation of innate immune response genes in their brain including IFITM1, IFITM2, Mx1 and STAT1 as well as MHC class I molecules [117]. The induction of immune response factors following VEEV exposure has also been observed in patient samples. Specifically, blood samples from individuals vaccinated with live attenuated VEEV TC-83 revealed transcriptomic alterations in multiple immune pathways at Days 3 and 7 post-vaccination, including interferon response, interferon-response factors, activation of pattern recognition receptors, and engagement of the inflammasome [118]. However, it is important to note that this study examined the response to VEEV vaccination and transcriptomic studies from human VEEV pathogenic cases have not been performed.