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Unraveling the mechanisms of HIV-induced hearing loss
  Oct 1 2022
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The prevalence of hearing loss among HIV seropositive patients has been shown to be alarmingly high compared with the general population. Studies have reported that 24% [1] of children and 49% [2] of adults with HIV demonstrate clinically significant hearing loss. HIV can affect nearly any tissue in the body, including the sensory and supporting cells of the inner ear that can lead to hearing loss. Recent studies have demonstrated that there is over a two-fold increase in the prevalence of sensorineural hearing loss (SNHL) in HIV-infected individuals compared with uninfected control groups [3]. The clinical manifestations of auditory disorders in HIV-positive patients mirror those in the general population including tinnitus (26%), vertigo (25%), hearing loss (27.5%), otalgia (19%), and ear canal pruritus (38%) [4]. Currently, limited data exist regarding the underlying molecular mechanisms involved in HIV-induced hearing loss.
It has been proposed that HIV has a multifocal effect on auditory perception (Fig. 1). Studies have postulated that HIV infection may first lead to synaptic loss, followed by cochlear damage and central disease, as the virus induces local inflammation and degeneration of auditory structures (Fig. 1) [5]. It has thus been suggested that all individuals presenting with HIV infection should undergo assessment of hearing function by otoacoustic emission (OAE) testing, pure tone and speech audiometry, speech-in-noise tests, or auditory brainstem recording measurements [5].
There are several factors that need to be investigated in the interplay of HIV and SNHL. Recent studies have shown that HIV-infected individuals demonstrate high morbidity of chronic SNHL. The ototoxicity of HAART [6] and separating its effects from HIV-induced hearing loss has been superficially explored [7,8]. HIV-positive patients have been shown to have increasingly abnormal OAE in higher frequencies as the duration of HAART treatment increases [9]. Higher rates of complications, including chronic otitis media, were also observed to be more common in HAART-treated HIV-positive children compared with matched controls [10]. As HAART has been shown to be toxic to multiple organ systems, it is necessary to further explore the effects of the therapy on hearing outcomes. Although HAART therapy has been shown to influence SNHL [11], there is currently no literature differentiating hearing outcomes of patients who are on HAART therapy versus those that are not. Furthermore, there is limited data regarding the ototoxic effects of the various classes of HAART, including nucleosides, nucleoside analog reverse transcriptase inhibitors, nonnucleoside analog reverse transcriptase inhibitors, and protease inhibitors, and their individual effects on SNHL susceptibility. There is a need to identify which HAART medications may have ototoxic side effects and to avoid those medications or reduce their dose in patients who are already suffering from mild to moderate hearing loss. Once identified, there is also a need to determine whether the duration of HAART use plays a role in SNHL.
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