Abstract
Marek’s disease (MD) in chickens is caused by Gallid alphaherpesvirus 2, better known as MD herpesvirus (MDV). Current vaccines do not block interindividual spread from chicken-to-chicken, therefore, understanding MDV interindividual spread provides important information for the development of potential therapies to protect against MD, while also providing a natural host to study herpesvirus dissemination. It has long been thought that glycoprotein C (gC) of alphaherpesviruses evolved with their host based on their ability to bind and inhibit complement in a species-selective manner. Here, we tested the functional importance of gC during interindividual spread and host specificity using the natural model system of MDV in chickens through classical compensation experiments. By exchanging MDV gC with another chicken alphaherpesvirus (Gallid alphaherpesvirus 1 or infectious laryngotracheitis virus; ILTV) gC, we determined that ILTV gC could not compensate for MDV gC during interindividual spread. In contrast, exchanging turkey herpesvirus (Meleagrid alphaherpesvirus 1 or HVT) gC could compensate for chicken MDV gC. Both ILTV and MDV are Gallid alphaherpesviruses; however, ILTV is a member of the Iltovirus genus, while MDV is classified as a Mardivirus along with HVT. These results suggest that gC is functionally conserved based on the virus genera (Mardivirus vs. Iltovirus) and not the host (Gallid vs. Meleagrid).
Highlights
All avian herpesviruses are members of the Alphaherpesvirinae within the Herpesviridae [1] and include Gallid alphaherpesviruses (GaHV) 1, 2, and 3 and Meleagrid alphaherpesvirus1 (MeHV-1), better known as infectious laryngotracheitis virus (ILTV) or GaHV-1, Marek’s disease herpesvirus (MDV) or GaHV-2, GaHV-3, and turkey herpesvirus (HVT), respectively
All contact birds in the v∆glycoprotein C (gC)-Con (Trial 1) and vILTVgC-Con (Trials 1 and 2) groups were negative for infection. These data show that both HVT gC and HVT gC with a C-terminal Myc-His tag were able to facilitate natural infection of MDV, while ILTV gC was unable to compensate for MDV gC
Utilizing our model for examining the essential role gC proteins play during interindividual spread in chickens [3,4,5,6,7,25] we sought to test the specificity of avian gC proteins
Summary
All avian herpesviruses are members of the Alphaherpesvirinae within the Herpesviridae [1] and include Gallid alphaherpesviruses (GaHV) 1, 2, and 3 and Meleagrid alphaherpesvirus1 (MeHV-1), better known as infectious laryngotracheitis virus (ILTV) or GaHV-1, Marek’s disease herpesvirus (MDV) or GaHV-2, GaHV-3, and turkey herpesvirus (HVT), respectively. MDV, GaHV-3, and HVT are classified into the genus Mardivirus, while ILTV is classified as an Iltovirus based on genomic sequencing [2]. Infection in the respiratory system is initiated by inhalation of infectious material in dander and dust that contains infectious virus previously shed from feather follicle (FF) epithelial (FFE) skin cells of infected birds. The most well studied Mardivirus is MDV where transmission of MDV can be through direct bird-to-bird contact or through indirect contact with infected feathers, dust, or dander. It is not completely understood what mechanism is used by MDV to spread in a flock; MDV glycoprotein C (gC)
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