Molecular Dissection of the Humoral Immune Response to Individual Varicella-Zoster Viral Proteins During Chickenpox, Quiescence, Reinfection, and Reactivation

The development of the humoral immune response against porcine reproductive and respiratory syndrome (PRRS) virus was monitored by an indirect fluorescent antibody (IFA) test, immunoperoxidase monolayer assay (IPMA), enzyme-linked immunosorbent assay (ELISA), and serum virus neutralization (SVN) test over a 105-day period in 8 pigs experimentally infected with ATCC strain VR-2402. Specific antibodies against PRRS virus were first detected by the IFA test, IPMA, ELISA, and the SVN test 9-11, 5-9, 9-13, and 9-28 days postinoculation (PI), respectively, and reached their maximum values by 4-5, 5-6, 4-6, and 10-11 weeks PI, respectively, thereafter. After reaching maximum value, all assays showed a decline in antibody levels. Assuming a constant rate of antibody decay, it was estimated by regression analysis that the ELISA, IFA, IPMA, and SVN antibody titers would approach the lower limits of detection by approximately days 137, 158, 324, and 356 PI, respectively. In this study, the immunoperoxidase monolayer assay appeared to offer slightly better performance relative to the IFA test, ELISA, and SVN test in terms of earlier detection and slower rate of decline in antibody titers. Western immunoblot analysis revealed that antibody specific for the 15-kD viral protein was present in all pigs by 7 days PI and persisted throughout the 105-day observation period. Initial detection of antibodies to the 19-, 23-, and 26-kD proteins varied among pigs, ranging from 9 to 35 days PI. Thereafter, the antibody responses to these 3 viral proteins of PRRS virus continued to be detected throughout the 105-day study period. These results clearly indicate that the 15-kD protein is the most immunogenic of the 4 viral proteins identified and may provide the antigenic basis for the development of improved diagnostic tests for the detection of PRRS virus antibodies.

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

Journal of Veterinary Diagnostic Investigation ◽

10.1177/104063879000200107 ◽

1990 ◽

Vol 2 (1) ◽

pp. 35-43 ◽

Cited By ~ 5

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.

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Humoral Immune Response to Measles, Varicella-Zoster and Tetanus Vaccination in Preterm Infants

Pediatric Research ◽

10.1038/pr.2011.710 ◽

2011 ◽

Vol 70 ◽

pp. 485-485

Author(s):

C F Schlindwein ◽

M C A A Perin ◽

M I de Moraes-Pinto ◽

R Simão ◽

A F M A Mimica ◽

...

Keyword(s):

Immune Response ◽

Preterm Infants ◽

Humoral Immune Response ◽

Varicella Zoster ◽

Humoral Immune ◽

Tetanus Vaccination

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Humoral immune response to HSV-1 and HSV-2 viral proteins in patients with primary genital herpes

Journal of Medical Virology ◽

10.1002/jmv.1890170208 ◽

1985 ◽

Vol 17 (2) ◽

pp. 153-166 ◽

Cited By ~ 51

Author(s):

Rhoda Ashley ◽

Jacqueline Benedetti ◽

Lawrence Corey

Keyword(s):

Immune Response ◽

Genital Herpes ◽

Humoral Immune Response ◽

Viral Proteins ◽

Humoral Immune ◽

Hsv 1

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Antigen-Specific B-Cell Responses to Porcine Reproductive and Respiratory Syndrome Virus Infection

Journal of Virology ◽

10.1128/jvi.01023-07 ◽

2007 ◽

Vol 82 (1) ◽

pp. 358-370 ◽

Cited By ~ 50

Author(s):

Prasad Mulupuri ◽

Jeffrey J. Zimmerman ◽

Joseph Hermann ◽

Craig R. Johnson ◽

Jean Paul Cano ◽

...

Keyword(s):

Immune Response ◽

B Cell ◽

Humoral Immune Response ◽

Viral Proteins ◽

Respiratory Syndrome Virus ◽

Humoral Immune ◽

Cell Responses ◽

B Cell Responses ◽

Over Time

ABSTRACT Porcine reproductive and respiratory syndrome virus (PRRSV) causes an acute, viremic infection of 4 to 6 weeks, followed by a persistent infection lasting for several months. We characterized antibody and B-cell responses to viral proteins in acute and persistent infection to better understand the immunological basis of the prolonged infection. The humoral immune response to PRRSV was robust overall and varied among individual viral proteins, with the important exception of a delayed and relatively weak response to envelope glycoprotein 5 (GP5). Memory B cells were in secondary lymphoid organs, not in bone marrow or Peyer's patches, in contrast to the case for many mammalian species. Potent anti-PRRSV memory responses were elicited to recall antigen in vitro, even though a second infection did not increase the B-cell response in vivo, suggesting that productive reinfection does not occur in vivo. Antibody titers to several viral proteins decline over time, even though abundant antigen is known to be present in lymphoid tissues, possibly indicating ineffective antigen presentation. The appearance of antibodies to GP5 is delayed relative to the resolution of viremia, suggesting that anti-GP5 antibodies are not crucial for resolving viremia. Lastly, viral infection had no immunosuppressive effect on the humoral response to a second, unrelated antigen. Taking these data together, the active effector and memory B-cell responses to PRRSV are robust, and over time the humoral immune response to PRRSV is effective. However, the delayed response against GP5 early in infection may contribute to the prolonged acute infection and the establishment of persistence.

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