Marek's disease virus infection in the brain: virus replication, cellular infiltration, and major histocompatibility complex antigen expression

Marek's disease virus (MDV) infection in the brain was studied chronologically after inoculating 3-week-old chickens of two genetic lines with two strains of serotype I MDV representing two pathotypes (v and vv+). Viral replication in the brain was strongly associated with the development of lesions. Three viral antigens (pp38, gB, and meq) were detected in the brain of infected chickens. Marked differences between v and vv+ pathotypes of MDV were identified for level of virus replication, time course of brain lesions, and expression of major histocompatibility complex (MHC) antigens. Two pathologic phenomena (inflammatory and proliferative) were detected in the brain of chickens inoculated with vv+MDV, but only inflammatory lesions were observed in those inoculated with vMDV. Inflammatory lesions, mainly composed of macrophages, CD4+ T cells, and CD8+ T cells, started at 6-10 days postinoculation (dpi) and were transient. Proliferative lesions, characterized by severe infiltrates of CD4+CD8- T cells (blasts), started at 19-26 dpi and persisted. Expression of MHC antigens in endothelial cells and infiltrating cells within the brain was influenced by MDV infection. Upregulation of MHC class II antigen occurred in all treatment groups, although it was more severe in those inoculated with vv+MDV. MHC class I antigen was downregulated only in those groups inoculated with vv+MDV. These results enhance our understanding of the nature and pattern of MDV infection in the brain and help to explain the neurovirulence associated with highly virulent MDV.     

Serologic evidence in commercial chicken and turkey flocks of infection with reticuloendotheliosis virus

A serologic survey has documented probable infection with reticuloendotheliosis (RE) virus in 21.0% of 101 layer flocks, 23.5% of 85 broiler and broiler-breeder flocks, 2.3% of 43 backyard chicken flocks, and 4.8% of 125 turkey production and breeder flocks. However, no infection was detected in 72 grandparent lines of chicken breeding stocks representing meat-type and layer strains. The existence of natural infection was further supported by isolation of RE virus from one experimental chicken flock and two commercial turkey flocks. This study supports earlier but subsequently discounted data by Aulisio and Shelokov that exposure to RE virus occurs commonly among commercial chickens in the United States, as has also been reported in other countries.     

Effects of chemically or virus-induced immunodepression on response of chickens to avian leukosis virus

The effects of chemically or virus-induced immunodepression on the infection profile (development of viremia and antibody) and shedding of avian leukosis virus (ALV) were studied in progeny chickens of experimental or commercial breeder flocks. Chickens were infected with ALV subgroup A by contact at hatching and by oral inoculation at 4-5 weeks of age. In the first experiment, chickens were inoculated with a virulent strain of infectious bursal disease virus (IBDV) at 1 day or 6 weeks of age. In the second experiment, chickens were neonatally treated with cyclophosphamide (CY), or were inoculated with strain T of reticuloendotheliosis virus (REV) at hatching, or were inoculated with strain JM of Marek's disease virus (MDV) at 2 weeks of age. The infection profile and cloacal shedding of ALV in chickens exposed to ALV and inoculated with immunodepressive viruses or CY were compared with those in hatchmates exposed only to ALV. In two of four chicken lines tested in the first experiment, shedding of ALV, as determined by virological assays of cloacal swabs at 22 weeks of age, was significantly higher in chickens infected with IBDV at 1 day of age than in uninfected hatchmates. The rate of shedding of ALV in one of these two lines was also significantly higher in chickens infected with IBDV at 6 weeks of age than in uninfected chickens. Further, the frequency of ALV-antibody detection at 22 weeks of age was significantly lower in chickens of these two lines infected with IBDV at 1 day of age than in uninfected chickens. In the second experiment, neonatal treatment with CY significantly increased the frequency of viremic chickens of both experimental and commercial flocks. The frequency of ALV-viremic chickens at 22 weeks of age was considerably higher in the REV- and MDV-inoculated groups (54% and 44%, respectively) than in control hatchmates (29%), but only in chickens of the commercial line. These findings suggest that chemically or virus-induced immunodepression may lead to an increase in rates of viremia and shedding of ALV in chickens infected with virus after hatching, especially in certain genetic lines.     

New serotype 2 and attenuated serotype 1 Marek's disease vaccine viruses: selected biological and molecular characteristics

Two new Marek's disease vaccine viruses, Md11/75C/R2 (serotype 1) and 301B/1 (serotype 2), were evaluated in chickens with maternal antibodies (ab+) or without maternal antibodies (ab-). Strain Md11/75C/R2 was mildly pathogenic in ab--chickens, but this pathogenicity was markedly reduced in ab+ chickens. Md11/75C/R2 spread less by contact and replicated better, both in vivo and in vitro, than CVI988/C, another serotype 1 vaccine virus. Strain 301B/1 was similar to SB-1, another serotype 2 vaccine virus: both were nonpathogenic for ab--chickens, spread readily by contact, and replicated well in vivo. In vitro, 301B/1 grew more rapidly and produced larger plaques than SB-1. Notable characteristics of strain CVI988/C included absence of pathogenicity, poor replicative ability, and the absence of one epitope detected by a common serotype-1-specific monoclonal antibody. All four viruses could be distinguished from each other by restriction enzyme analysis of viral DNA. We conclude that Md11/75C/R2, although exceptionally protective, may require further attenuation. On the other hand, 301B/1, which in other studies induced higher levels of protection than SB-1, is nonpathogenic and may be considered for use as a commercial vaccine.     

Conjunctive representation of position, direction, and velocity in entorhinal cortex

Grid cells in the medial entorhinal cortex (MEC) are part of an environment-independent spatial coordinate system. To determine how information about location, direction, and distance is integrated in the grid-cell network, we recorded from each principal cell layer of MEC in rats that explored two-dimensional environments. Whereas layer II was predominated by grid cells, grid cells colocalized with head-direction cells and conjunctive grid x head-direction cells in the deeper layers. All cell types were modulated by running speed. The conjunction of positional, directional, and translational information in a single MEC cell type may enable grid coordinates to be updated during self-motion-based navigation.