Genetic Evolution And Analyses Of Rotavirus Prevalent In Neonates

Objective: To monitor rotavirus(RV) infection and the genetic characteristics among neonates in 2015, to analyze the genetic changes of major epidemic strains of RV in neonates from 1996 to 2015, to explore its origin and evolution, to build a data foundation for the prevention and treatment of RV infection among neonates. Methods: A total of 818 stool samples were collected from diarrheal and non-diarrheal neonates hospitaled in People’s Hospital of Xinjiang Uygur Autonomous Region in 2015. The general and clinical data of all the neonates were collected, SPSS17.0 was used to analyze relevant parameters. RV antigen was detected with ELISA. RV positive samples were further genotyped for G and P by multiplex RT PCR. The VP7 and VP4 genes of prevalent strains from 1996 to 2014 preserved and 2015 were sequenced, MEGA6.0 software was used to draw phylogenetic dendrograms to analyze the changes and evolution trends. Whole genome sequencing of the most prevalent strains with G3P[6] in 2006 were carried out and whole genome genotypes and origin were confirmed. Results: Positive rate for RV was 7.58% among neonates in 2015. RV detection rate of diarrheal neonates was significantly higher than it of non-diarrheal neonates(2? =68.496,P<0.05). G9P[6] was the predominant genotype. Phylogenetic analysis revealed the 9 strains with G2 in 1996-2003 were in two evolutionary clusters, the nucleotide homologies among strains were 97.7%~100%. The 31 strains with G9 in 2004-2015 were also in two evolutionary clusters and the nucleotide homologies among strains were 97.6%~100%. The 37 strains with P[6] belonged to five different branches, the nucleotide homologies among strains were 96.6%~100%. More than one strain with the same genotype could be detected in the same year, possessed the characteristics of continuous transmission and moved at spiral with times in both G and P genotypes. Three G3P[6] strains in 2006 belonged to Wa-like genegroup, with the genotype constellation feature of G3-P[6]-I1-R1-C1-M1-A1-N1-T1-E1-H1, it might result from the gene reassortment or mutation between the infant G3P[8] and neonatal G9P[P6], and then got relative enhancement in its virulence enough to cause an epidemic among neonates. Conclusion: G9P[6] was still the predominant genotype among neonates in 2015. The most likely origin of G3P[6] strains in 2006 was from human RV strains through reassortment or mutation. The gene variances of neonate RV strains revealed a small fluctuation and were in a state of slow spiral upward and adaptive survival evolution. RV infection could be detected stablely over a long period of time. It is necessary to monitor RV infection and to be alert to RV infection among neonates with new genotypes and nosocomial outbreak, emerging from gene reassortment or mutation by mixed RV infection between infants and neonates.