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31 December 2025

BoGHV-4 Genotypic Diversity Shapes Inflammatory and Viral Gene Expression in Platelet-Rich Plasma-Supplemented Bovine Endometrial Cells

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1
Instituto de Innovación para la Producción Agropecuaria y el Desarrollo Sostenible (IPADS) (INTA–CONICET), Ruta 226, km 73.5, Balcarce B7620, Buenos Aires, Argentina
2
Facultad de Ciencias Agrarias, Universidad Nacional de Mar del Plata, Ruta 226, km 73.5, Balcarce B7620, Buenos Aires, Argentina
3
Laboratorio Álvarez, 25 de Mayo 139, Bahía Blanca B8000, Buenos Aires, Argentina
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Escola Superior de Agricultura Luiz de Queiroz, Universidad de São Pablo, Piracicaba CEP 13418-900, Brazil
This article belongs to the Special Issue Animal Herpesvirus 2025

Abstract

Bovine gammaherpesvirus 4 (BoGHV-4) is an opportunistic uterine pathogen whose reactivation is associated with postpartum inflammation and bacterial lipopolysaccharide (LPS). Platelet-rich plasma (PRP) is a regenerative biotherapeutic capable of modulating inflammatory responses, although its effects may vary depending on BoGHV4 genotype. In this study, primary bovine endometrial cells (BECs) were cultured in medium containing 10% PRP instead of fetal bovine serum, infected with two genetically divergent BoGHV-4 isolates (07-435, genotype 3; 10-154, genotype 2), and subsequently stimulated with bacterial lipopolysaccharide (LPS, 100 ng/mL). Expression of the viral immediate-early gene IE-2 and host immune genes (TLR4, TNF-α, CXCL8, and IFN-γ) were quantified by RT-qPCR from 4 to 48 h after stimulation. Isolate 07-435 induced a sustained activation of IE-2 and gradual cytokine upregulation, while isolate 10-154 elicited an early but transient inflammatory response followed by gene downregulation. PRP did not modify the strain-specific patterns of viral and inflammatory gene expression but established a common inflammatory baseline, whereas the magnitude and temporal profile of the response continued to be dictated by the viral genotype. These findings indicate that BoGHV-4 genotypic diversity remained the main determinant of response intensity and duration, supporting PRP as a context-dependent rather than a universal antiviral modulator.

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