Introduction
Chikungunya fever is featured as an acute febrile illness and associated to a severe and debilitating polyarthralgias.[1]Caused by Chikungunya virus (CHIKV), that belong of theTogaviridae family and genus Alphavirus, discovered in 1950s in Tanzania on the African continent, the name Chikungunya derivate from the idiom Makonde, that means ”that which bends up”, due to the severe polyarthralgia that make the infected people walk with a stooped posture, with the spine curved. This virus is transmitted by the bite of an infected mosquito of the genus Aedes to humans. CHIKV virus is small, with icosahedral symmetry and a capsid size of 65-70 nanometers in diameter. The viral genome consists of a single positive-strand RNA molecule, 12 kb-long with a methylguanosine cap at 5´ UTR (untranslated region) and a polyadenylated at 3´ UTR. It has two ORF (open reading frame). One that encode for non-structural proteins involved in virus replication and pathogenesis, and other encodes for structural proteins that compose the virion structure.[2] Phylogenetic inferences on the envelope protein (E1) gene sequences suggest that the virus Chikungunya can be subdivided in three genotypes: (i) Asian, (ii) East/Central/South/African (ECSA), and (iii) West African.[3–5]
In 2004, CHIKV re-emerged and spread to new regions, such as Europe, and caused millions of infections throughout countries in the Indian subcontinent. It has been proposed that the introduction of CHIKV into new area and its current worldwide distribution has been facilitated by: (i) the high attack rates associated high levels of viremia in infected humans,[9] and, (ii) the high competence of theAedes spp vectors, responsible for transmitting CHIKV in epidemiologic settings.[1,5,6]
Serum levels of the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST) are elevated in several diseases, such as chronic viral hepatitis, non-alcoholic fatty liver disease, autoimmune hepatitis, hemochromatosis, and alcoholic liver disease. Therefore, both are taken as markers of liver damage. On the other hand, creatinine and urea are renal markers that indicate renal injury levels.[7]
Moreover, high levels of uric acid are a well-established risk factor for gout and renal problems.[8,9] Clinical and laboratory evidence indicated muscular dysfunctions in patients infected by Dengue virus (DENV), with high blood levels of creatine kinase (CK), enzyme that indicate muscular lesion.[9] Likewise, CHIKV infects progenitor muscular cells, which associates with muscle tissue damage.[9]
In infections caused by other arboviruses such as DENV and Yellow Fever virus (YFV), changes in liver enzymes are observed, due to viral tropism for hepatocytes, which causes cell death and an increase in ALT and AST levels in the serum. Although clinical studies evidenced the severe complications during CHIKV infection [10], in our work we tried describe the course of infection in eighty-six CHIKV-viremic patients. Therefore, we evaluated clinical findings comparing to biochemical test results for: (i) hepatic enzymes, such as alanine aminotransferase and aspartate aminotransferase (ALT, AST) and, (ii) renal markers, such as: urea, creatinine and uric acid.