tetano
Editor, Senior Moderator
J Gen Virol. 2012 Sep 5. [Epub ahead of print]
Quantification of heterosubtypic immunity between avian influenza subtypes H3N8 and H4N6 in multiple avian host species.
Pepin KM, Vandalen KK, Mooers NL, Ellis JW, Sullivan HJ, Root JJ, Webb CT, Franklin AB, Shriner SA.
Source
Fogarty International Center, Bethesda, MD, USA;
Abstract
Low-pathogenicity avian influenza viruses (LPAIV) can lead to epizootics that cause economic losses in poultry or the emergence of human-infectious strains. LPAIVs experience a complex immunity landscape since they are endemic in multiple host species and many antigenically-distinct strains co-circulate. Prevention and control of emergence of detrimental strains requires an understanding of infection/transmission characteristics of multiple subtypes in multiple hosts, including interactions between subtypes. In order to develop analytical frameworks for examining control efficacy, quantification of heterosubtypic immunity interactions is fundamental. However, these data are scarce, especially for wild avian subtypes in natural hosts. Consequently, we infected three host species (mallards, quail and pheasants) with two LPAIV subtypes isolated from wild birds: H3N8 and H4N6. We also re-infected recovered hosts with the alternate subtype to measure effects of heterosubtypic immunity. We collected oropharyngeal and cloacal swabs and quantified viral RNA load by real-time RT-PCR. For secondary infections in recovered hosts, peak viral load was up to four orders of magnitude lower, and shedding length was up to 4 days shorter. However, both the magnitude and presence of heterosubtypic immunity varied across specific host species-subtype combinations. Using a mathematical model of viral replication, we quantified the variation in viral replication dynamics due to host individuals. We found that accounting for individual heterogeneity is important for drawing accurate conclusions about treatment effects. Our results are relevant for developing epidemiological models to inform control practices and for analyzing viral replication data.
PMID:
22956733
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22956733
Quantification of heterosubtypic immunity between avian influenza subtypes H3N8 and H4N6 in multiple avian host species.
Pepin KM, Vandalen KK, Mooers NL, Ellis JW, Sullivan HJ, Root JJ, Webb CT, Franklin AB, Shriner SA.
Source
Fogarty International Center, Bethesda, MD, USA;
Abstract
Low-pathogenicity avian influenza viruses (LPAIV) can lead to epizootics that cause economic losses in poultry or the emergence of human-infectious strains. LPAIVs experience a complex immunity landscape since they are endemic in multiple host species and many antigenically-distinct strains co-circulate. Prevention and control of emergence of detrimental strains requires an understanding of infection/transmission characteristics of multiple subtypes in multiple hosts, including interactions between subtypes. In order to develop analytical frameworks for examining control efficacy, quantification of heterosubtypic immunity interactions is fundamental. However, these data are scarce, especially for wild avian subtypes in natural hosts. Consequently, we infected three host species (mallards, quail and pheasants) with two LPAIV subtypes isolated from wild birds: H3N8 and H4N6. We also re-infected recovered hosts with the alternate subtype to measure effects of heterosubtypic immunity. We collected oropharyngeal and cloacal swabs and quantified viral RNA load by real-time RT-PCR. For secondary infections in recovered hosts, peak viral load was up to four orders of magnitude lower, and shedding length was up to 4 days shorter. However, both the magnitude and presence of heterosubtypic immunity varied across specific host species-subtype combinations. Using a mathematical model of viral replication, we quantified the variation in viral replication dynamics due to host individuals. We found that accounting for individual heterogeneity is important for drawing accurate conclusions about treatment effects. Our results are relevant for developing epidemiological models to inform control practices and for analyzing viral replication data.
PMID:
22956733
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22956733