Affiliation:
1. Postgraduate Program in Parasitic Biology of the Amazon Center for Biological and Health Sciences University of the State of Pará Belém Pará Brazil
2. Department of Arbovirology and Hemorrhagic Fever Instituto Evandro Chagas Ministry of Health Ananindeua Pará Brazil
3. Postgraduate Program in Virology Instituto Evandro Chagas Ananindeua Pará Brazil
Abstract
AbstractThe chikungunya virus (CHIKV) is a member of the genus Alphavirus, family Togaviridae. CHIKV causes an acute systemic febrile condition, accompanied by severe polyarthralgia, intense muscle pain, and maculopapular exanthema, which may still occur in many patients. In rare cases, unusual symptoms may occur, eventually worsening the condition and resulting in a fatal outcome. It is a single‐stranded, non‐segmented RNA virus with a genome of approximately 11,805 nucleotides that organises a genetic and molecular chain that encodes non‐structural proteins (nsP1, nsP2, nsP3, nsP4) and structural proteins (E3, E2, 6K, and E1). The fundamental role of immune response in the evolution of the disease is known. Understanding the role of immune response in the pathogenesis of CHIKV infection is challenging. In this context, innate and adaptive immune responses establish a connective interface that induces the production of various mediators that modulate the strategy of inhibiting viral replication. However, the immune escape articulated by the virus indicates that the action of pro‐and anti‐inflammatory cytokines contributes to the worsening of the disease and potentiates tissue damage with joint involvement. In this review, we discuss the role of the primary pro‐and anti‐inflammatory cytokines in the immunopathological processes of chikungunya fever.
Funder
Conselho Nacional de Desenvolvimento Científico e Tecnológico
Subject
Infectious Diseases,Virology
Cited by
3 articles.
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