Research and Reports in Immunology

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Research Article - Research and Reports in Immunology (2022) Volume 5, Issue 1

In a mouse tumor model, it provided better protection than the standard MVA.

Amelia Kelly*

Department of Microbiology and Immunology, The University of Melbourne, Parkville, Victoria, Australia

*Corresponding Author:
Amelia Kelly
Department of Microbiology and Immunology
The University of Melbourne
Victoria, Australia

Received: 30-Jan-2022, Manuscript No. AARRI-22-56896;  Editor assigned 2- Feb -2022, PreQC No. AARRI-22-56896 (PQ); Reviewed:  15- Feb-2022, QC No AARRI-22-56896; Revised: 18- Feb -2022, Manuscript No. AARRI-22-56896(R); Published: 25- Feb -2022, DOI: 10.35841/aarri-5.1.104

Citation: Kelly A. In a mouse tumour model, it provided better protection than the standard MVA. Res Rep Immunol. 2022;5(1):104


African horse sickness, AHSVMVA-VP2, Protection, Humoral immunity, Passive immunization.

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Previous research has found that a recombinant Modified Vaccinia Ankara (MVA) virus expressing AHSV serotype 4 VP2 (MVA-VP2) elicited virus neutralizing antibodies in horses and protected interferon alpha receptor gene knock-out mice from challenge. Passive transfer of antiserum from MVA-VP2 immune donors to recipient mice afforded complete clinical protection and considerably lowered viraemia, according to follow-up tests. These investigations have been expanded to see if MVA-VP2 vaccine-induced antiserum has a protective effect when given as a challenge. In addition, splenocytes were passively transferred to immunologically naive recipient mice to see if they conferred any immunity. Antisera and splenocytes were obtained from groups of mice that had received MVA-VP2 or wild type MVA vaccinations for passive immunization of recipient animals. Following that, the animals were challenged with AHSV-4 (along with corresponding vaccinated or unvaccinated control animals), and protection was determined by comparing clinical symptoms, mortality, and viraemia between the treatment and control groups. Even in immunized mice, all antiserum recipients demonstrated high illness survival rates and statistically significant reductions in viraemia when compared to the control groups. When comparing mice who received splenocytes from MVA-VP2 vaccinates to those who received splenocytes from MVA-wt vaccinates, the mice who received splenocytes from MVA-VP2 vaccinates showed just a minor reduction in viraemia and only a survival rate. These findings support the notion that protective immunity imparted by MVA-VP2 vaccination is predominantly humoral in origin, and they point to the possibility of using MVA-VP2 specific antiserum as an emergency treatment for AHSV.


Immune characteristics of HIV/AIDS vaccine candidates that may be important in HIV-1 infection prevention are still unknown. One of the most promising vectors for use as an HIV-1 vaccine is the highly attenuated poxvirus strain MVA. We previously discovered a recombinant MVA (referred to as MVA-B) that produced HIV-1-specific immune responses in diverse animal models and gene signatures in human dendritic cells (DCs) with immunoregulatory function. The horse is the most seriously affected species by African horse sickness (AHS), an arthropod-borne viral disease of solipeds carried by haematophagous insects of the genus Culicoides [1][2].

AHSV epidemics in immunologically naive populations can result in high mortality rates. African horse sickness virus (AHSV) isolates, strains, and serotypes are all categorised as part of the species African horse sickness virus, genus Orbivirus, family Reoviridae. Bluetongue virus, which causes bluetongue disease in ruminants, is closely linked to AHSV. Orbiviruses have a genome made up of 10 linear dsRNA segments, with one copy of each segment packaged into each viral particle [3]. The spherical, non-enveloped capsid of AHSV is made up of three concentric protein layers and measures about diameter. The outer-capsid layer is principally involved in cell attachment and entrance and is formed by two important structural proteins, VP2 and VP5 (encoded by genome segments 2 and 6 respectively). AHSV's VP2 antigen is the most variable and is responsible for serotype definition. Infection with AHSV causes severe clinical illness and death in horses, yet those who survive develop a strong, lifelong but serotype-specific immunity. Virus neutralising antibodies (VNAb) have been linked to the humoral character of AHS immunity in both horses and mice using colostrum and monoclonal antibodies, respectively. Following the challenge, the animals were observed twice daily and more frequently (at least three times per day) if any signs of morbidity appeared, such as changes in behaviour and activity, changes in water or food intake, changes in the appearance of the hair coat, body weight loss, presence of ocular signs (conjunctivitis, ocular discharge, swelling), changes in hydration, and the presence of neurological signs. (i.e. paresis, paralysis, ataxia). Permanent hunching, acute conjunctivitis, evidence of dehydration, loss of more than half of body weight, presence of any neurological abnormalities, or any other condition that prohibited food or drink intake were among the compassionate end-points for euthanasia [4][5]. Animals with any of these clinical symptoms were humanely euthanized by cervical dislocation after isoflurane anaesthesia.


In this investigation, the highly protective impact of antiserum produced from MVA-VP2 vaccinated mice was demonstrated even when transferred post-infection, confirming earlier findings. When the antiserum dose was raised, the protective effect was remarkably similar to that seen in MVA-VP2 vaccinated mice that were actively immunised. The few clinical indications that remained in infected mice before transfer vanished over time, and the animals recovered entirely. This shows that passive immunisation with MVAVP2 antiserum could be employed for therapeutic purposes, such as the treatment of AHS in horses in the early phases of an outbreak before containment or extensive vaccination campaigns are implemented.


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