Abstract

Congenital cytomegalovirus (CMV) infection induces a clinical syndrome usually associated with hearing loss. However, the effect of acquired CVM infection in adults and children has not been clearly defined. The objective of this review is to critically appraise scientific evidence regarding the association of acquired CMV infection with postnatal hearing loss or tinnitus. A systematic review of records reporting sensorineural hearing loss (SNHL) or tinnitus and acquired CMV infection including articles published in English was performed. Search strategy was limited to human studies with acquired CMV infection. After screening and quality assessment, nine studies involving 1528 individuals fulfilled the inclusion criteria. A total of 14% of patients with SNHL showed evidence of previous exposure to CMV, while in individuals without SNHL (controls) the percentage rose up to 19.3%. SNHL was reported as unilateral or bilateral in 15.3%, and not specified in 84.7% of cases. The degree of SNHL ranged from mild to profound for both children and adults. None of the records reported tinnitus. The prevalence of children or adults with acquired SNHL with a confirmed acquired CMV infection by Polymerase Chain Reaction (PCR) or IgM anti-CMV antibodies is low. Phenotyping of patients with acquired CMV infection was limited to hearing loss by pure tone audiometry and no additional audiological testing was performed in most of the studies. Additional symptoms deserve more attention, including episodic vertigo or tinnitus, since some patients with the clinical spectrum of Meniere Disease could result from a CMV latent infection.

Highlights

  • The human cytomegalovirus (CMV) is a DNA virus included in the herpesviridae family, widely spread in the community

  • The aim of the study is to critically appraise scientific evidence regarding the association of acquired CMV infection with postnatal hearing loss or tinnitus

  • The discarded records were non-human studies or abstracts presented at scientific meetings

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Summary

Introduction

The human cytomegalovirus (CMV) is a DNA virus included in the herpesviridae family, widely spread in the community. Congenital CMV infection can produce a wide variety of clinical syndromes either by direct pathogenic effect or secondary to immune mechanisms. The viral genome is maintained in the host cell without active replication; CMV is able to reactivate itself in response to changes in the host cell [2]. CMV persists for the lifetime of the infected host leading to a latent chronic infection, in which only a limited number of viral genes are expressed without genome replication. Cellular death pathways that are activated by viral infection as well as other biological processes, including control of the cell cycle and cellular stress responses, are efficiently regulated by CMV in the infected cell to facilitate virus replication. CMV has a broad cellular tropism and infects a large number of cell types during primary infection; the outcome of infection varies widely and is largely cell type-dependent and it may include endothelial, epithelial, fibroblasts, neuronal, monocytes/macrophages, granulocytes, and smooth muscle cells [3]

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