Cell-Mediated Responses to Human Metapneumovirus Infection.

Marlies Ballegeer,Xavier Saelens

doi:10.3390/v12050542

Marlies Ballegeer, Xavier Saelens

Open Access

https://doi.org/10.3390/v12050542

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Abstract

Viruses are the most common cause of acute respiratory tract infections (ARTI). Human metapneumovirus (hMPV) frequently causes viral pneumonia which can become life-threatening if the virus spreads to the lungs. Even though hMPV was only isolated in 2001, this negative-stranded RNA virus has probably been circulating in the human population for many decades. Interestingly, almost all adults have serologic evidence of hMPV infection. A well-established host immune response is evoked when hMPV infection occurs. However, the virus has evolved to circumvent and even exploit the host immune response. Further, infection with hMPV induces a weak memory response, and re-infections during life are common. In this review, we provide a comprehensive overview of the different cell types involved in the immune response in order to better understand the immunopathology induced by hMPV. Such knowledge may contribute to the development of vaccines and therapeutics directed against hMPV.

Highlights

Acute respiratory tract infections (ARTI) are the most common cause of symptomatic illness worldwide
Supporting that, nearly 100% of people test positive for antibody reactivity in their blood by the age of 10, and almost all adults have serologic evidence of prior human metapneumovirus (hMPV) infection [3,20,21,22]. hMPV is classified into two major genetic lineages, hMPV A and B, that are further subdivided into lineages A1, A2, B1, and B2 [3,23,24]
One crucial aspect of the development of vaccines or therapeutics is the knowledge of host immune responses to hMPV infection and understanding of the immunopathology induced by the virus

Summary

Introduction

Acute respiratory tract infections (ARTI) are the most common cause of symptomatic illness worldwide. A viral infection induces IFN-dependent antiviral defense strategies in AECs. As a counteraction, viruses modulate this response via several mechanisms resulting in inhibition of IFN synthesis, affecting type I IFN responses and blocking the expression of ISGs [67]. Several transcriptomic studies focused on the many upregulated genes that are involved in the initiation of pro-inflammatory and antiviral immune responses, including chemokines, cytokines, type I IFN, and interferon-inducible proteins [59,64,80]. HMPV infection causes tricarboxylic acid (TCA) cycle impairment and drives de novo fatty acid synthesis which has been shown to be necessary for replication of several viruses [83] Another interesting observation was the fact that hMPV induced a progressive decrease of antioxidant enzyme (AOE) expression levels in AECs and the lungs of infected mice.

Neutrophils

B Cells

Findings

Conclusions