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.