Respiratory syncytial virus (RSV) is a major cause of lower respiratory tract infections in infants and young children. RSV is characterised by high variability, especially in the G glycoprotein, which may play a significant role in RSV pathogenicity by allowing immune evasion. To reconstruct the origin and phylodynamic history of RSV, we evaluated the genetic diversity and evolutionary dynamics of RSV A and RSV B isolated from children under 3 years old infected in Italy from 2006 to 2012. Phylogenetic analysis revealed that most of the RSV A sequences clustered with the NA1 genotype, and RSV B sequences were included in the Buenos Aires genotype. The mean evolutionary rates for RSV A and RSV B were estimated to be 2.1×10(-3) substitutions (subs)/site/year and 3.03×10(-3) subs/site/year, respectively. The time of most recent common ancestor for the tree root went back to the 1940s (95% highest posterior density-HPD: 1927-1951) for RSV A and the 1950s (95%HPD: 1951-1960) for RSV B. The RSV A Bayesian skyline plot (BSP) showed a decrease in transmission events ending in about 2005, when a sharp growth restored the original viral population size. RSV B BSP showed a similar trend. Site-specific selection analysis identified 10 codons under positive selection in RSV A sequences and only one site in RSV B sequences. Although RSV remains difficult to control due to its antigenic diversity, it is important to monitor changes in its coding sequences, to permit the identification of future epidemic strains and to implement vaccine and therapy strategies.

Phylogeny and population dynamics of respiratory syncytial virus (Rsv) A and B / M. Martinelli, E.R. Frati, A. Zappa, E. Ebranati, S. Bianchi, E. Pariani, A. Amendola, G. Zehender, E. Tanzi. - In: VIRUS RESEARCH. - ISSN 0168-1702. - 189:(2014 Jun 19), pp. 293-302. [10.1016/j.virusres.2014.06.006]

Phylogeny and population dynamics of respiratory syncytial virus (Rsv) A and B

M. Martinelli;E.R. Frati;A. Zappa;E. Ebranati;S. Bianchi;E. Pariani;A. Amendola;G. Zehender;E. Tanzi
2014

Abstract

Respiratory syncytial virus (RSV) is a major cause of lower respiratory tract infections in infants and young children. RSV is characterised by high variability, especially in the G glycoprotein, which may play a significant role in RSV pathogenicity by allowing immune evasion. To reconstruct the origin and phylodynamic history of RSV, we evaluated the genetic diversity and evolutionary dynamics of RSV A and RSV B isolated from children under 3 years old infected in Italy from 2006 to 2012. Phylogenetic analysis revealed that most of the RSV A sequences clustered with the NA1 genotype, and RSV B sequences were included in the Buenos Aires genotype. The mean evolutionary rates for RSV A and RSV B were estimated to be 2.1×10(-3) substitutions (subs)/site/year and 3.03×10(-3) subs/site/year, respectively. The time of most recent common ancestor for the tree root went back to the 1940s (95% highest posterior density-HPD: 1927-1951) for RSV A and the 1950s (95%HPD: 1951-1960) for RSV B. The RSV A Bayesian skyline plot (BSP) showed a decrease in transmission events ending in about 2005, when a sharp growth restored the original viral population size. RSV B BSP showed a similar trend. Site-specific selection analysis identified 10 codons under positive selection in RSV A sequences and only one site in RSV B sequences. Although RSV remains difficult to control due to its antigenic diversity, it is important to monitor changes in its coding sequences, to permit the identification of future epidemic strains and to implement vaccine and therapy strategies.
Evolutionary rate; G protein; Phylodynamic analysis; Phylogenetic analysis; Respiratory syncytial virus; Selective pressure
Settore MED/42 - Igiene Generale e Applicata
Settore MED/17 - Malattie Infettive
Settore MED/07 - Microbiologia e Microbiologia Clinica
19-giu-2014
Article (author)
File in questo prodotto:
Non ci sono file associati a questo prodotto.
Pubblicazioni consigliate

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/238619
Citazioni
  • ???jsp.display-item.citation.pmc??? 17
  • Scopus 32
  • ???jsp.display-item.citation.isi??? 29
social impact