Anamnestic Immune Response of Pigs to Pseudorabies Virus: Latent Virus Reactivation versus Direct Oronasal and Parenteral Exposure to Virus

1991 ◽  
Vol 3 (2) ◽  
pp. 133-136 ◽  
Author(s):  
W. L. Mengeling
Keyword(s):  
Immune Response ◽  
Pseudorabies Virus ◽  
Latent Virus ◽  
Virus Reactivation ◽  
Parenteral Exposure

scholarly journals Sequential Changes in the Humoral Immune Response of Pigs to Pseudorabies Virus after Vaccination, Exposure to Virulent Virus, and Reactivation of Latent Virus

1990 ◽  
Vol 2 (1) ◽  
pp. 35-43 ◽  
Author(s):  
William L. Mengeling ◽  
Eugene C. Pirtle
Keyword(s):  
Immune Response ◽  
Humoral Immune Response ◽  
Pseudorabies Virus ◽  
Viral Proteins ◽  
Latent Virus ◽  
Virus Reactivation ◽  
Dexamethasone Treatment ◽  
Humoral Immune ◽  
Attenuated Virus ◽  
Virulent Virus

Sequential changes in the humoral immune response of pigs to pseudorabies virus (PRV) after each of several exposures to the virus were evaluated by determining virus neutralization (VN) and radioimmunoprecipitation (RIP) activities of sera collected at selected intervals. Pigs were vaccinated intramuscularly with live attenuated virus (6 pigs), inactivated attenuated virus (6 pigs), or inactivated virulent virus (6 pigs). All pigs were challenged oronasally with virulent virus 3 weeks later and 12 (4 pigs of each vaccine group) were subsequently treated with dexamethasone in an attempt to reactivate latent virus. The relatively low serum titers of VN antibody that were raised by vaccination (titers ranged from 2 to 32) increased markedly (at least 16-fold) for all pigs after exposure to virulent virus. After dexamethasone treatment, the VN titers of 2 pigs increased 16-fold, whereas those of the other 10 dexamethasone-treated pigs and the 6 nontreated pigs either remained the same or increased only minimally (i.e., no more than 2-fold). The results of RIP using 35S-methionine-labeled viral proteins were initially similar to those of VN in that the low levels of serum RIP activity detected after vaccination increased markedly after subsequent exposure to virulent virus. In contrast to VN, however, most pigs (11 of 12) treated with dexamethasone had a clear increase in serum RIP activity. The increase was particularly striking for viral proteins of relatively low (<46K) molecular weight. Precipitating activity for 14C-glucosamine-labeled viral glycoproteins was not detected until after pigs were exposed to virulent virus. The increase in RIP activity detected after dexamethasone treatment was likely due to an additional antigenic stimulus associated with virus reactivation. However, virus was isolated from nasal swabs of only 4 of the 12 treated pigs. None of the results appeared to be affected appreciably by the type of vaccine used for initial immunization.

scholarly journals Effects of a porcine reproductive and respiratory syndrome virus infection on the development of the immune response against pseudorabies virus

2000 ◽  
Vol 76 (1-2) ◽  
pp. 125-135 ◽  
Author(s):  
M.G.M De Bruin ◽  
J.N Samsom ◽  
J.J.M Voermans ◽  
E.M.A van Rooij ◽  
Y.E De Visser ◽  
...  
Keyword(s):  
Immune Response ◽  
Virus Infection ◽  
Pseudorabies Virus ◽  
Respiratory Syndrome Virus

scholarly journals CMV-Specific Immune Response—New Patients, New Insight: Central Role of Specific IgG during Infancy and Long-Lasting Immune Deficiency after Allogenic Stem Cell Transplantation

2019 ◽  
Vol 20 (2) ◽  
pp. 271 ◽  
Author(s):  
Przemyslaw Zdziarski
Keyword(s):  
Immune Response ◽  
Nk Cells ◽  
Cellular Immune Response ◽  
Specific Immune Response ◽  
Primary Immune Response ◽  
Virus Reactivation ◽  
Allogenic Stem Cell Transplantation ◽  
Specific Igg ◽  
Cellular Immune

Although the existing paradigm states that cytomegalovirus (CMV) reactivation is under the control of the cellular immune response, the role of humoral and innate counterparts are underestimated. The study analyzed the host–virus interaction i.e., CMV-immune response evolution during infection in three different clinical situations: (1) immunodeficient CMV-positive human leukocyte antigen (HLA)-matched bone marrow recipients after immunoablative conditioning as well as immunocompetent, (2) adult, and (3) infant with primary immune response. In the first situation, a fast and significant decrease of specific immunity was observed but reconstitution of marrow-derived B and natural killer (NK) cells was observed prior to thymic origin of T cells. The lowest CMV-IgG (93.2 RU/mL) was found just before CMV viremia. It is noteworthy that the sole and exclusive factor of CMV-specific immune response is a residual recipient antibody class IgG. The CMV-quantiferon increase was detected later, but in the first phase, phytohemagglutinin (PHA)-induced IFN-γ release was significantly lower than that of CMV-induced (“indeterminate” results). It corresponds with the increase of NK cells at the top of lymphocyte reconstitution and undetected CMV-specific CD8 cells using a pentamer technique. In immunocompetent adult (CMV-negative donor), the cellular and humoral immune response increased in a parallel manner, but symptoms of CMV mononucleosis persisted until the increase of specific IgG. During infancy, the decrease of the maternal CMV-IgG level to 89.08 RU/mL followed by clinical sequel, i.e., CMV replication, were described. My observations shed light on a unique host-CMV interaction and CMV-IgG role: they indicate that its significant decrease predicts CMV replication. Before primary cellular immune response development, the high level of residual CMV-IgG (about >100 R/mL) from mother or recipient prevents virus reactivation. The innate immune response and NK-dependent IFN-secretion should be further investigated.

Improved immune response to an attenuated pseudorabies virus vaccine by ginseng stem-leaf saponins (GSLS) in combination with thimerosal (TS)

2016 ◽  
Vol 132 ◽  
pp. 92-98 ◽  
Author(s):  
Jingxuan Ni ◽  
Shicheng Bi ◽  
Wei Xu ◽  
Cenrong Zhang ◽  
Yisong Lu ◽  
...  
Keyword(s):  
Immune Response ◽  
Virus Vaccine ◽  
Pseudorabies Virus ◽  
Stem Leaf

scholarly journals Effects of mild stress on the immune response against pseudorabies virus in mice

1999 ◽  
Vol 67 (2) ◽  
pp. 153-160 ◽  
Author(s):  
J de Groot ◽  
H.W.M Moonen-Leusen ◽  
G Thomas ◽  
A.T.J Bianchi ◽  
J.M Koolhaas ◽  
...  
Keyword(s):  
Immune Response ◽  
Pseudorabies Virus ◽  
Mild Stress

Abstract # 1855 Latent virus reactivation in astronauts during international space station

2016 ◽  
Vol 57 ◽  
pp. e40-e41
Author(s):  
S.K. Mehta ◽  
M.L. Laudenslager ◽  
R.P. Stowe ◽  
B.E. Crucian ◽  
A.H. Feiveson ◽  
...  
Keyword(s):  
International Space Station ◽  
Space Station ◽  
Latent Virus ◽  
Virus Reactivation ◽  
International Space

Bryostatin-1 for latent virus reactivation in HIV-infected patients on antiretroviral therapy

AIDS ◽  
2016 ◽  
Vol 30 (9) ◽  
pp. 1385-1392 ◽  
Author(s):  
Carolina Gutiérrez ◽  
Sergio Serrano-Villar ◽  
Nadia Madrid-Elena ◽  
Maria J. Pérez-Elías ◽  
Maria Elena Martín ◽  
...  
Keyword(s):  
Antiretroviral Therapy ◽  
Latent Virus ◽  
Virus Reactivation ◽  
Bryostatin 1

scholarly journals Suppression of the Interferon-Mediated Innate Immune Response by Pseudorabies Virus

2006 ◽  
Vol 80 (13) ◽  
pp. 6345-6356 ◽  
Author(s):  
Alla Brukman ◽  
L. W. Enquist
Keyword(s):  
Immune Response ◽  
Cell Activation ◽  
Pseudorabies Virus ◽  
Nk Cell ◽  
Innate Immune ◽  
Human Pathogens ◽  
Wild Type ◽  
Varicella Zoster ◽  
Simplex Virus ◽  
Hsv 1

ABSTRACT Pseudorabies virus (PRV) is an alphaherpesvirus related to the human pathogens herpes simplex virus type 1 (HSV-1) and varicella-zoster virus. PRV is capable of infecting and killing a wide variety of mammals. How it avoids innate immune defenses in so many hosts is not understood. While the anti-interferon (IFN) strategies of HSV-1 have been studied, little is known about how PRV evades the IFN-mediated immune response. In this study, we determined if wild-type PRV infection can overcome the establishment of a beta interferon (IFN-β)-induced antiviral state in primary rat fibroblasts. Using microarray technology, we found that the expression of a subset of genes normally induced by IFN-β in these cells was not induced when the cells were simultaneously infected with a wild-type PRV strain. Expression of transcripts associated with major histocompatibility complex class I antigen presentation and NK cell activation was reduced, while transcripts associated with inflammation either were unaffected or were induced by viral infection. This suppression of IFN-stimulated gene expression occurred because IFN signal transduction, in particular the phosphorylation of STAT1, became less effective in PRV-infected cells. At least one virion-associated protein is involved in inhibition of STAT1 tyrosine phosphorylation. This ability to disarm the IFN-β response offers an explanation for the uniform lethality of virulent PRV infection of nonnatural hosts.

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