Viremia in Equine Herpes Virus-1 infection and a possible link to Transient Protective Immunity

Abstract

Equine herpes virus (EHV-1) causes respiratory infections in equine, and results in abortion, paresis, neonatal death, and retinopathy and the virus may become latent following initial infection. Virus entry is via the respiratory route, and the virus replicates in the host in ciliated and non-ciliated epithelial cells of the respiratory tract and in Type 1 and Type 2 pneumocytes in the lung parenchyma. After viral replication in the respiratory system, the virus can become disseminated to other parts of body via viraemic cells. The virus also can cross the placenta which leads to abortion of live or dead fetuses without premonitory signs. Infected horses show transient immunity after natural or experimental infection and immune responses to EHV-1, but the immunoprotective status begins to decline after a few months of active infection. Due to the transient immune response, recovered horses are not immunoprotected and thus are prone to subsequent re-infection. Immunity is not long lived after experimental or natural infection, and as a result the development of an effective vaccine has remained a challenge. In this study viraemic cells were studied in a murine EHV-1 infection model. Mice were infected intranasally and viraemic cells were studied on days three and five which occurs during the peak of the infection. The results of this study may help to identify the nature of viraemic cells and their role in the transient immune response to infection. Buffy coat cells and lungs were removed and stained with a fluorescent antibody test for EHV-1 antigen, and lung specimens were subjected to transmission electron microscopy. Both techniques confirmed the presence of viraemic cells in lung tissues. These viraemic cells were further stained for EHV-1 antigen, and for CD4 or CD8 biomarkers and results are discussed re: pathogenesis of EHV-1 infection, identification of viraemic cells in a murine model and possible link of viraemia to transient immune responses in EHV-1 infection, which demonstrate the validity of this murine model for the investigation of the cytopathologic mechanism and sequelae of EHV manifestation in this model.

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“…8 As with many viruses including influenza and the common cold, the coronaviruses are also subject to periodic mutation, thereby generating multiple epigenetic forms of the virus and which variants may result in variations of symptoms observed in the originating COVID-19 virus. 8,14,[21][22][23][24] Of concern, emerging coronavirus mutations may partially elude current vaccine and treatment protocols, and thus may enable the virus to continue to remain in circulation and remain infectious. The most recent variants, the Delta and the Omicron, have an even larger genome and more spike protein mutations than previous iterations, and have been reported to be more transmissible than previous variants, with up to 70% or more of new cases appearing to be caused by this latest variant on the spike protein.…”

An Editorial overview and Perspective: Can the attenuated Omicron variant of Covid-19 virus resolve the pandemic in 2022?

“…Ref The recent recommendations for administration of booster immunizations six or months after initial Immunization or exposure lends credibility and traction as such boosters may re-engage the immune system soon enough after administration and enabling the memory B cells of plasma and bone marrow to become reawakened, thereby improving circulating antibody levels to a more protective level should re-exposure occur during the immediate weeks and months following the booster re-immunization. It is not yet known if additional boosters beyond the firstyear may be in order in the future [21][22][23][24][25].…”