Latent Turkey Herpesvirus Infection in Lymphoid, Nervous, and Feather Tissues of Chickens

Abstract

In earlier studies, we found that a late gene product, glycoprotein B (gB) was highly expressed in lymphoid tissues of chickens inoculated with turkey herpesvirus (HVT). The objectives of the present study were twofold. First, we wanted to expand on our previous research and determine if gB expression declines or disappears during later time periods of HVT infection. Second, we wanted to correlate gB expression with presence of HVT, i.e. if gB expression is absent, can HVT still be detected? Fifteen 1-day-old chicks were inoculated by intraperitoneal inoculation with 2000 plaque forming units of strain FC126 HVT. Thymus, spleen, bursa, brachial plexus, sciatic plexus, and feather tips were harvested at 21, 28, 35, 70, and 105 days postinoculation (PI). Brachial plexus and sciatic plexus were examined at 21, 28, and 35 days PI, and feather tips were examined at 21 and 28 days PI. An indirect immunofluorescence assay was used to detect HVT gB expression, and an in situ hybridization assay was used to detect HVT. At 21 days PI, gB expression was present in the thymus, spleen, and bursa. At 28 and 35 days PI, gB expression was detected in the thymus and spleen. At 70 days PI, gB expression was detected only in the spleen, and at 105 days PI, gB expression was not detected in any of the lymphoid tissue (thymus, spleen, or bursa). gB expression was not detected in the brachial plexus, sciatic plexus, or feather tips at any of the five time points. The bursa contained HVT only at 21 and 28 days PI. However, HVT was demonstrated in all other tissues from 21 to 105 days PI. Progression from a productive HVT infection to a latent HVT infection results in the loss of gB expression. Throughout this progression, a region of the HVT genome can be detected by appropriate methods.

Complete, Long-Lasting Protection against Lethal Infectious Bursal Disease Virus Challenge by a Single Vaccination with an Avian Herpesvirus Vector Expressing VP2 Antigens

“…Fully productive infection results in production of infectious viruses in FFE cells, whereas productive-restrictive infection produces nonenveloped, noninfectious viruses in some lymphoid and epithelial cells. Latent infection occurs predominantly in T (16). In addition to these infection stages, the Pec promoter might leakily express the antigen in latently infected T cells, although most viral and foreign promoters are suppressed in the activated T cells (6,29).…”

Marek’s disease virus and skin interactions

“…Since the 1990s, new methods based on molecular biology techniques have appeared, enabling mardivirus genome detection (PCR) [47,48] and quantification (qPCR) [49-52]. It is also possible to detect viral DNA in feathers by pulse field gel electrophoresis (PFGE) [53] or via in situ hybridization [54]. An inexpensive and rapid method of amplification of the viral genome called LAMP (loop-mediated isothermal amplification) has been recently developed to allow rapid diagnostic in field conditions [55].…”

Herpesvirus Connection in the Expression of Autoimmune Vitiligo in Smyth Line Chickens

“…2). HVT is an a-herpesvirus that belongs to a group of Marek's disease viruses (MDV) (11,14). MDVs include three serotypes: MDV serotype-1 (MDV-1) consists of oncogenic viruses and their attenuated derivatives; MDV serotype 2 (SB2) consists of related non-oncogenic viruses isolated from chickens; and MDV serotype 3 (HVT) consists of non-oncogenic viruses isolated from turkeys.…”

“…HVT is used as a vaccine in chickens to protect chickens from MDV-1. Although oncogenic and non-oncogenic MDVs affect a variety of tissues (peripheral nerves, gonads, eye, viscera, muscle, and skin) to different degrees, they all exhibit special tropism for feather tissue where melanocytes are located (11,14). Additionally, lymphoid infiltration into the feather of MDV-infected birds resembles that observed in vitiliginous feathers (3,6,11), although pigmentation loss is normally not associated with MDV infection in chickens (11,14).…”

“…Although oncogenic and non-oncogenic MDVs affect a variety of tissues (peripheral nerves, gonads, eye, viscera, muscle, and skin) to different degrees, they all exhibit special tropism for feather tissue where melanocytes are located (11,14). Additionally, lymphoid infiltration into the feather of MDV-infected birds resembles that observed in vitiliginous feathers (3,6,11), although pigmentation loss is normally not associated with MDV infection in chickens (11,14). These characteristics of HVT and related viruses, together with the direct association between HVT and vitiligo incidence reported here, strongly support a role of HVT as an environmental factor in the expression of SL vitiligo.…”