We detected vertical transmission of chikungunya virus (CHIKV) in wild populations of Aedes aegypti from San Marcos, Guerrero, Mexico, with real-time reverse transcriptase-polymerase chain reaction. A total of 20 pools (1-11 specimens/pool) of larvae, male, and female mosquitoes were tested. We report the detection of CHIKV in 2 of 11 larval pools, 4 of 5 male pools, and 1 of 4 female pools, from field-collected mosquitoes.
Chikungunya is a public health problem in Africa, Asia, and Latin America. Innate immune response (IIR) possesses enzymatic cleavage of nucleic acids of the agent as an important mechanism of viral counteraction. Oligoadenylate synthetase (OAS) enzymes are key regulators of RNase L to develop IIR against RNA viruses. OAS´ Single Nucleotide Polymorphisms (SNPs) have been related to susceptibility toward RNA-virus diseases. A cross-sectional study was done of 187 patients. OAS1 SNPs (rs1131454), OAS2 SNPs (rs1293762, rs15895, and rs1732778) and OAS3 SNPs (rs2285932 and rs2072136) genes were studied by qPCR in check and symptomatic patients to associate SNPs with susceptibility to disease. Relative risk (RR), Chi2, and Hardy-Weinberg equilibrium indicated p < 0.05 statistical significance. SNPs rs1131454 and rs1293762 showed statistically significant differences between cases and check. Homozygous genotypes GG of rs1131454 and CC of rs1293762 were considered risk factors (RR 1.59; 95% CI 1.19-2.14 and RR 1.91; 95% CI 1.31-2.78, respectively). Heterozygous genotypes GA of rs1131454 and AC of rs1293762 were protective factors (RR 0.67; 95% CI 0.48-0.94 and RR 0.56; 95% CI 0.37-0.83, respectively). Moreover, rs1293762 was statistically significant in allelic frequencies between cases and checks, with A allele a protective factor (RR = 0.55; 95% CI 0.39-.078) and C allele a susceptibility factor (RR = 1.80; 95% CI difference (p < 0.05) in the allelic frequencies between cases and checks, with A allele as protection factor (RR = 1.28-2.54). Our results add to previously reported evidence of susceptibility of certain populations with specific OAS-family SNPs against CHIKV.
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