Genetic variability in envelope-associated protein genes of closely related group A strains of respiratory syncytial virus

Zheng, HaoQiang; Storch, Greg A.; Zang, Chunyi; Peret, Teresa C. T.; Park, Chung S.; Anderson, Larry J.

doi:10.1016/s0168-1702(98)00132-4

Cited by 25 publications

(17 citation statements)

References 19 publications

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“…The previous studies regarding the antigenic and genetic variability of the F protein have had limitations, including the fact that these studies had been conducted on the basis of limited numbers of strains, and also that they employed strains which were either geographically or chronologically widely separated. Also, little attention has been paid to the relationship between surface proteins with regard to genetic variation, except in the studies conducted by Zheng et al [1999] and Cane and Pringle [1991]. For a better understanding of the J. Med.…”

Section: Discussionmentioning

confidence: 99%

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Genetic variability of the fusion protein and circulation patterns of genotypes of the respiratory syncytial virus

Kim

Choi

Lee

2007

Journal of Medical Virology

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Although antigenic and genetic variations were shown to occur both in the G and F protein of respiratory syncytial virus (RSV), few studies looked at the variation of F gene. The F genotypes were determined by the evaluation of clustering patterns, via the phylogenetic analysis of the nucleotide sequences of a variable region in the F gene. One hundred seventy-nine strains obtained from a children's hospital in Korea over nine consecutive epidemics were included. The relationship between the F and G genotypes was analyzed with the G genotypes previously published by the authors. The phylogenetic analysis of the variable region from the F gene revealed 9 genotypes among 129 group A RSVs and 4 genotypes among 50 group B RSVs. In each of the epidemics, the dominant genotypes were replaced with new genotypes in consecutive epidemics. In each of the epidemics of group B RSVs, the predominant genotype alternated between genotypes. Most of the strains which clustered to a particular F genotype were assigned to particular G genotype(s). By determining the nearly entire sequences of the F genes, we revealed the percentage of the nucleotide differences which resulted in amino acid coding changes was determined to be much great in two distinct variable regions of the F gene. Our results indicated that the F gene of the RSVs may be continuously evolving under selective pressure in a distinct pattern, and that the genetic variability of the F protein is associated with that of the G protein.

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Section: Discussionmentioning

confidence: 99%

“…According to the literature, the greatest divergence of the F gene occurs within the F2 subunit [Johnson and Collins, 1988;Zheng et al, 1999]. Based on these reports, the 550 nucleotides of the F gene (23-572 nucleotides of the N terminal region) were sequenced initially for all of the isolates.…”

Section: Nucleotide Sequencingmentioning

confidence: 99%

Genetic variability of the fusion protein and circulation patterns of genotypes of the respiratory syncytial virus

Kim

Choi

Lee

2007

Journal of Medical Virology

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“…A third example comes from sequence analysis of RSV isolates, in which a segment of the SH gene of several isolates of one genetic lineage appeared to be derived from a second lineage (27). This suggested that the polymerase had jumped over, copied part of the SH gene, and jumped back.…”

Section: Discussionmentioning

confidence: 99%

Genetic Recombination during Coinfection of Two Mutants of Human Respiratory Syncytial Virus

Spann

Collins

Teng

2003

J Virol

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Recombination between coinfecting viruses had not been documented previously for a nonsegmented negative-strand RNA virus (mononegavirus). We investigated the potential of intermolecular recombination by respiratory syncytial virus (RSV) by coinfecting HEp-2 cells with two recombinant RSV (rRSV) mutants lacking either the G gene (⌬G/HEK) or the NS1 and NS2 genes (⌬NS1/2). These viruses replicate inefficiently and form pinpoint plaques in HEp-2 cells. Therefore, potential recombined viruses with a growth and/or plaque formation advantage should easily be identified and differentiated from the two parental viruses. Further identification of potential recombinants was aided by the inclusion of point mutation markers in the F and L genes of ⌬G/HEK and the design of reverse transcription-PCR (RT-PCR) primers capable of detecting these markers. Independent coinfections and control single infections by these two rRSV mutants were performed. In one of six coinfections, an RSV variant was identified that produced plaques slightly larger than those of wild-type RSV in HEp-2 cells. RT-PCR and sequencing provided evidence that this variant was a recombined RSV (rec-RSV). The rec-RSV appeared to have been generated by a polymerase jump from the ⌬G/HEK genome to that of ⌬NS1/2 and back again in the vicinity of the SH-G-F genes. This apparently involved nonhomologous and homologous recombination events, respectively. The recombined genome was identical to that of the ⌬G/HEK mutant except that all but the first 12 nucleotides of the SH gene were deleted and replaced by an insert consisting of the last 91 nucleotides of the G gene and its downstream intergenic region. This insert could have come only from the coinfecting ⌬NS1/2 virus. This resulted in the formation of a short chimeric SH:G gene. Northern and Western blot analysis confirmed that the rec-RSV did not express the normal SH and G mRNAs and proteins but did express the aberrant SH:G mRNA. This provides an experimental demonstration of intermolecular recombination yielding a viable, helper-independent mononegavirus. However, the isolation of only a single rec-RSV under these optimized conditions supports the idea that RSV recombination is rare indeed.

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“…Comparison of sequences from G genes from geographically and temporally diverse RSV clinical specimens suggests cumulative genetic change, representing a genetic drift pattern [Zheng and Storch, 1999]. This contributes to the transience seen in RSV immunity, since re-infection throughout life is a common occurrence, which typically presents as a mild upper respiratory tract infection in adults.…”

Section: Introductionmentioning

confidence: 99%

Molecular epidemiological analysis of a nosocomial outbreak of respiratory syncytial virus associated pneumonia in a kangaroo mother care unit in South Africa

Visser¹,

Delport²,

Venter³

2008

Journal of Medical Virology

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Respiratory syncytial virus (RSV) may cause severe lower respiratory tract disease in premature infants. Prolonged viral shedding has been reported in patients with underlying immunosuppressive disorders, such as human immunodeficiency virus 1 (HIV-1) infection. During March to May 2006, 23 preterm pediatric patients developed nosocomial pneumonia in a district hospital in the Gauteng Province of South Africa due to RSV infection. The patients were identified using routine diagnostic testing. All had been admitted with their mothers to a Kangaroo Mother Care (KMC) ward from birth--a low care unit for the management of stable low birth weight infants. The HIV-1 seroprevalence among the mothers to these infants was 52.6%, translating to a 52.6% perinatal exposure. A multiplex nested RT-PCR was used to subtype RSV positive nasopharyngeal aspirates. Sequencing and phylogenetic analysis of part of the G-protein gene was used for molecular epidemiological analysis of the outbreak. In total, 19 of the 23 RSV positive specimens could be PCR amplified and sequenced. The subtype A, GA5 genotype was identified in 14 specimens and the BA genotype, a new subtype B genotype not previously recognized in South Africa, in seven. One patient had an infection with both genotypes. Phylogenetic analysis demonstrated eight separate introductions. Two of the strains identified in this outbreak were identical to strains circulating in a general pediatric ward of this hospital during the preceding month. Inadequate infection control measures by health care providers and mothers to children in KMC units may increase potentially the risk of severe RSV infection in a population group with compounded risk factors.

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Genetic variability in envelope-associated protein genes of closely related group A strains of respiratory syncytial virus

Cited by 25 publications

References 19 publications

Genetic variability of the fusion protein and circulation patterns of genotypes of the respiratory syncytial virus

Genetic variability of the fusion protein and circulation patterns of genotypes of the respiratory syncytial virus

Genetic Recombination during Coinfection of Two Mutants of Human Respiratory Syncytial Virus

Molecular epidemiological analysis of a nosocomial outbreak of respiratory syncytial virus associated pneumonia in a kangaroo mother care unit in South Africa

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