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
1990 ◽  
Vol 2 (1) ◽  
pp. 35-43 ◽  
Author(s):  
William L. Mengeling ◽  
Eugene C. Pirtle

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.


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 ◽  
...  

2019 ◽  
Vol 20 (2) ◽  
pp. 271 ◽  
Author(s):  
Przemyslaw Zdziarski

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.


2016 ◽  
Vol 132 ◽  
pp. 92-98 ◽  
Author(s):  
Jingxuan Ni ◽  
Shicheng Bi ◽  
Wei Xu ◽  
Cenrong Zhang ◽  
Yisong Lu ◽  
...  

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 ◽  
...  

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

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 ◽  
...  

2006 ◽  
Vol 80 (13) ◽  
pp. 6345-6356 ◽  
Author(s):  
Alla Brukman ◽  
L. W. Enquist

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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