Presence Of Viral Antibodies Research Articles

Application of Localized Surface Plasmon Resonance of Conjugated Gold Nanoparticles in Spectral Diagnosis of SARS-CoV-2: A Numerical Study.

Severe respiratory syndrome COVID-19 (SARS-CoV-2) outbreak has became the most important global health issue, and simultaneous efforts to fast and low-cost diagnosis of this virus were performed by researchers. One of the most usual tests was colorimetric methods based on the change of color of gold nanoparticles in the presence of viral antibodies, antigens, and other biological agents. This spectral change can be due to the aggregation of the particles or the shift of localized surface plasmon resonance due to the electrical interactions of surface agents. It is known that surface agents could easily shift the absorption peak of metallic nanocolloids which is attributed to the localized surface plasmon resonance. Experimental diagnosis assays for colorimetric detection of SARS-CoV-2 using Au NPs were reviewed, and the shift of absorption peak was studied from the viewpoint of numerical analysis. Using the numerical method, the refractive index and real and imaginary parts of the effective relative permittivity of the viral biological shell around Au NPs were obtained. This model gives a quantitative description of colorimetric assays of the detection of SARS-CoV-2 using Au NPs.

West Nile Virus in Horses, Guatemala

To the Editor: West Nile virus (WNV, Flaviviridae: Flavivirus) is emerging as a public health and veterinary concern. Since its introduction into North America in 1999, it has spread rapidly, reaching the Caribbean Basin in 2001, Mexico in 2002, El Salvador in 2003, and Colombia in 2004 (1). However, reports of equine illness and deaths in Latin America are inconclusive. With the exception of viral isolates from a dead bird, a human, and a mosquito pool in Mexico (2,3), all reports of WNV presence in Latin America have relied on serologic evidence. WNV is a member of the Japanese encephalitis serocomplex, which in the Western Hemisphere includes St. Louis encephalitis virus (SLEV) (4). Serologic investigations for WNV in Latin America must use highly specific assays to differentiate WNV infection from potentially cross-reactive viruses such as SLEV or possibly additional unknown viruses. In particular, SLEV is of concern since it was previously isolated from Guatemalan mosquitoes (5). Alerted by the findings of WNV transmission in the region (1), we collected serum samples from horses from 19 departments of Guatemala from September 2003 to March 2004, to initially estimate the extent of WNV spread and its potential public health risk. Because no animals exhibited signs of neurologic illness at the time of the survey, only healthy horses were sampled. Before 2005, equine WNV vaccines were prohibited and unavailable in Guatemala (Unidad de Normas y Regulaciones, Ministerio de Agricultura Ganaderia y Alimentacion, Guatemala, pers. comm.); as such, cross-reactivity due to prior vaccination is highly unlikely. Samples were initially tested for WNV-reactive antibodies by using an epitope-blocking enzyme-linked immunosorbent assay (blocking ELISA) (6). The ability of the test sera to block the binding of the monoclonal antibodies to WNV antigen was compared to the blocking ability of control horse serum without antibody to WNV. Data were expressed as relative percentages and inhibition values >30% were considered to indicate the presence of viral antibodies. A subset of positive samples was further confirmed by plaque-reduction neutralization test (7). Of 352 samples, 149 (42.3%) tested positive with the 3.1112G WNV-specific monoclonal antibody. Of 70 blocking ELISA–positive samples, the neutralization tests indicated the infecting agent was WNV, SLEV, and undifferentiated flavivirus in 9, 33, and 21 samples, respectively. Titers were expressed as the reciprocal of serum dilutions yielding >90% reduction in the number of plaques in a plaque-reduction neutralization test (PRNT90). PRNT90 titers of horses seropositive for WNV ranged from 80 to 320. PRNT90 titers of horses seropositive for SLEV ranged from 40 to 2,560. For the differential diagnosis of samples with neutralizing antibody titers against both WNV and SLEV in this test, a >4-fold titer difference was used to identify the etiologic agent. The undifferentiated flavivirus-reactive specimens had <4-fold difference in cross-neutralization titers. Likely possibilities for the inability to distinguish the infecting virus include previous infection with these or other flaviviruses (previously described or unknown) resulting in elevated cross-reactive titers. The remaining 10% of specimens that tested negative by PRNT probably represent nonneutralizing antibodies in the serum or false positivity in the blocking ELISA. Our serologic results provide indirect evidence of past transmission of WNV, SLEV, and possibly other flaviviruses to horses in Guatemala. Although no confirmed cases of WNV-attributed disease have been reported in Central America to date, flavivirus transmission appears to be widely distributed in Guatemala (Figure). Efforts are under way to confirm WNV transmission by viral isolation and to evaluate the impact of WNV on human, horse, and wildlife populations. More information is needed to establish the public health threat of WNV and other zoonotic flaviviruses in the region. Figure Geographic distribution in Guatemala of horses showing previous infections with West Nile virus (WNV), Saint Louis encephalitis virus (SLEV), or undifferentiated flavivirus as confirmed by plaque reduction neutralization test. Each location may have multiple ...

Isolation of a Fusion Protein Containing the Antigenic Domain 1 of Human Cytomegalovirus Glycoprotein B and its Application in ELISA Tests

The glycoprotein B (gB) of human cytomegalovirus represents a dominant antigen for the humoral immune response. The immunodominant region on gB is the antigenic domain 1 (AD-1), a complex structure that requires a minimal continuous sequence of more than 75 amino acids for antibody binding. In this study, this domain was expressed in Escherichia coli as a fusion protein with beta-galactosidase but yielded insoluble protein aggregates as inclusion bodies. To recover the fusion protein, inclusion bodies were solubilized by two extractions with urea 8 M: and the fusion protein then isolated using gel filtration chromatography. After confirmation of fusion protein antigenicity by Western blotting, the purified product was used as the capturing antigen in an enzyme-linked immunosorbent assay (ELISA) to determine the presence of viral antibodies in serum samples of pregnant women. A cut-off point of approximately 0.2 absorbance units could discriminate the results of seropositive from seronegative pregnant women. The data indicates the potential usefulness of the fusion protein for the development of immunoassay for detection of the HCMV antibodies.

Maternally derived humoral immunity to bovine viral diarrhea virus (BVDV) 1a, BVDV1b, BVDV2, bovine herpesvirus-1, parainfluenza-3 virus bovine respiratory syncytial virus, Mannheimia haemolytica and Pasteurella multocida in beef calves, antibody decline by half-life studies and effect on response to vaccination

The passive immunity transferred to calves from their dams was investigated in a beef herd to determine half-life of antibody, estimated time to seronegative status and effect on immunization. One hundred two beef calves in a commercial ranch under standard management conditions were utilized. Samples were collected at branding (day 0). This was the first possible date to collect samples postcalving. This was approximately 2 months postcalving, and days 95 and 116. The calves were divided into two groups: vaccinates (51) and nonvaccinates (51). The calves were vaccinated with a commercial inactivated viral vaccine containing bovine viral diarrhea virus (BVDV)1a, BVDV2, bovine herpesvirus-1 (BHV-1), parainfluenza-3 virus (PI-3V), and bovine respiratory syncytial virus (BRSV) on days 0 and 95. Half of the vaccinated and unvaccinated calves also received one dose of an experimental Mannheimia haemolytica and Pasteurella multocida vaccine at day 95. Serums were tested for neutralizing antibody titers to BVDV1a, BVDV1b, BVDV2, BHV-1, PI-3V, and BRSV. Antibodies were detected by ELISA to M. haemolytica whole cell, M. haemolytica leukotoxin, and P. multocida outer membrane protein (OMP). The mean half-life of viral antibodies in nonvaccinated calves to each virus was: BVDV1a, 23.1 days (d); BVDV1b, 22.8 d; BVDV2, 22.9 d; BHV-1, 21.2 d; PI-3V, 30.3 d; and BRSV, 35.9 d. The mean half-life of viral antibodies was greater for vaccinates than for nonvaccinates for all viruses except BRSV. The calculated mean time to seronegative status for nonvaccinates based on titers at day 0 was: BVDV1a, 192.2 d; BVDV1b, 179.1 d; BVDV2, 157.8 d; BHV-1, 122.9 d; PI-3V, 190.6 d; and BRSV, 186.7 d. There was an active immune response after vaccination with two doses to all the viruses, except BRSV. Mean antibody titers of vaccinates at day 116 were statistically higher than nonvaccinates for all viruses except BRSV. However on an individual calf basis there were few seroconversions (four-fold rise or greater to BVDV1a, BVDV1b, BVDV2, PI-3V, or BRSV; or two-fold rise for BHV-1) in the presence of viral antibodies. The predicted time of seronegative status for a group of calves for vaccination programs may not be appropriate as there may be a range of titers for all calves at day 0. In this study the range for BVDV1a was 16–16,384; BVDV1b, 8–8192; BVDV2, 0–8192; BHV-1, 0–935; PI-3V, 8–2048; and BRSV, 8–4096. Using the half-life of 23 d for BVDV1a, the time thereafter for seronegative status would be 46 and 299 d compared to the calculated date of 192.2 d using the mean of estimated time to seronegative status for all the calves. There was an active humoral response in the vaccinated calves to M. haemolytica and P. multocida. Cowherd humoral immunity based on serum antibodies should be monitored as it may relate to transfer of maternal antibodies to calves. Exceptionally high levels of viral antibodies transferred to calves could interfere with the antibody response to vaccination.

Cirrhosis of undefined pathogenesis: absence of evidence for unknown viruses or autoimmune processes.

To examine whether unknown viruses or autoimmune processes contribute to the development of cryptogenic liver disease, we studied 48 patients undergoing liver transplantation who had non-A, non-B cirrhosis; non-blood-borne cirrhosis of unknown etiology; or autoimmune cirrhosis. After the diagnosis of hepatitis C virus infection was established by the presence of viral antibodies or viral RNA, patients were reclassified into three groups: hepatitis C virus infection, autoimmune cirrhosis and cryptogenic cirrhosis. Explant histological appearance, incidence of posttransplant hepatitis and immunological features were compared in the three groups. Thirty-one percent of patients had neither hepatitis C virus infection nor classical autoimmune cirrhosis and were classified as having cryptogenic cirrhosis. Unlike histological appearance in hepatitis C virus infection but similar to that in autoimmune cirrhosis, explant histological appearance of cryptogenic cirrhosis showed inactive cirrhosis with little inflammation. After transplantation, histological hepatitis of the allograft was demonstrated in 44% of patients with hepatitis C infection but in no patient with autoimmune or cryptogenic cirrhosis. The autoimmune score, developed from clinical criteria associated with autoimmune liver disease, was significantly lower in cryptogenic cirrhosis and hepatitis C virus infection than in autoimmune cirrhosis. Autoantibodies--including antinuclear antibodies, smooth muscle antibodies and liver-kidney microsomal antibodies--were not commonly present in serum of patients with cryptogenic cirrhosis, whereas antibodies to soluble liver antigens were found with increased frequency in this entity. We conclude that in many patients with liver disease, no pathogenesis can be identified.(ABSTRACT TRUNCATED AT 250 WORDS)

Recurrent Peritonitis: Evidence for Possible Viral Etiology

A 45-year-old woman who was treated with continuous ambulatory peritoneal dialysis (CAPD) developed recurrent peritonitis characterized by cloudy effluents, elevated white blood cell (WBC) counts (predominantly lymphocytes), and negative culture results. This case report suggests that she may have had viral peritonitis as indicated by a positive viral culture, the presence of viral antibodies in serum and peritoneal dialysis effluent (PDE), hematological findings, and cell surface receptor studies. The possibility of a viral cause should be considered in patients with culture-negative peritonitis, especially if they do not respond to antibiotics.

1031 HEMOPHILIAC IMMUNODEFICIENCY: INFLUENCE OF EXPOSURE TO FACTOR VIII, HUMAN T LEUKEMIA VIRUS (HTLV III) AND HERPESVIRUSES

We have evaluated 121 patients with hemophilia A for cellular immune defects and exposure to HTLV III, Epstein-Barr Virus (EBV) and cytomegalovirus (CMV). Immunoregulatory defects were found in the majority of the patients studied: decreased OKT.4/T.8 ratio, decreased lymphocyte proliferation in response to phytohemagglutinin (PHA), anti-immunoglobulin, pokeweed mitogen (PWM) and streptolysin O, and decreased natural killer (NK) cell activity(p<.05). Delayed hypersensitivity skin test responses to a battery of 6 antigens were completely absent in 42% of patients. 70% of the population had antibodies to HTLV III, EBV and 43% to CMV. Multivariate analysis was performed at a confidence level of, p<.01 and demonstrated that the single most important predictor of immunoregulatory defects was the amount of Factor VIII used. Absolute numbers of T helper cells, helper/suppressor cell ratios, PHA and PWM responses were all negatively correlated with units/kg of Factor VIII utilized. Out of 10 correlations found between the presence of viral antibodies and immune abnormalities, 7 involved HTLV III alone or in combination with CMV and/or EBV; notably positive correlations with PHA, anti-immunoglobulin, T-suppressor cells. EBV correlated negatively with T-suppressor cell populations, while correlations with CMV occurred only in the presence of antibodies to EBV and/or HTLV III. These studies demonstrate that treatment of hemophilia with Factor VIII concentrate is associated with long-term immunoregulatory defects and that exposure to HTLV III plays a role in producing further defects.

Presence of viral antibodies to the human lymphoma-leukemia virus in patients with acquired immune deficiency syndrome.

Presence of viral antibodies to the human lymphoma-leukemia virus in patients with acquired immune deficiency syndrome.

Replication of murine coronaviruses in somatic cell hybrids formed between a mouse fibroblast cell line and either a rat Schwannoma line or a rat glioma line.

The murine hepatitis viruses can readily establish persistent infections both in vivo and in vitro. In vivo, persistent infections, dependent upon the virus strain, and the age and genetic background of the host, can occur resulting in chronic hepatitis or chronic demyelination of the central nervous system (1). In vitro, these agents can establish persistent infections in both neural and non-neural cell lines (2,3,4) without the requirements for viral modifications or environmental manipulations such as the presence of viral antibody or interferon.KeywordsCell HybridPersistent InfectionSomatic Cell HybridMouse Hepatitis VirusHypoxanthine Phosphoribosyl TransferaseThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Persistent cyclic herpes simplex virus infection in vitro. IV. Changes in the severity of the infections in the presence of antibody.

Hampar, Berge (National Institute of Dental Research, Bethesda, Md.). Persistent cyclic herpes simplex virus infection in vitro. IV. Changes in the severity of the infections in the presence of antibody. J. Bacteriol. 92:1741-1747. 1966.-The severity of persistent herpes simplex virus (HSV) infections maintained in the presence of viral antibody (AB) changed with time. These changes could be divided into three distinct phases during which the severity of the infections were maintained at low (phase 1), high (phase 2), and intermediate (phase 3) levels. Paralleling these changes was the appearance in the cultures of a new HSV variant which induced the formation of giant cells. The changes in the severity of the infections were attributable to three factors. The first was the presence in the cultures of virus-resistant cells. The second was the suppressive effects due to virus neutralization by the AB. The third was the inherent properties of each HSV variant which determined the amount of virus remaining in an infectious form in the presence of AB. Finally, the period of "exacerbation" in vitro (phase 2) was compared with recurrent episodes in human herpes infection.