Short Communication: Human Immunodeficiency Virus Rebound in Blood and Seminal Plasma Following Discontinuation of Antiretroviral Therapy

Dear Editor, We read the article entitled “Abnormal Dispersion of Ventricular Repolarization as a Risk Factor in Patients with Human Immunodeficiency Virus: Tp-e Interval, Tp-e/QTc Ratio” by Unal Evren et al. with interest[1]. The authors evaluated the changes in Tp-e interval, Tp-e/QT and Tp-e/corrected QT (QTc) ratios, and traditional electrocardiographic features of electrical dispersion in adults infected with Human Immunodeficiency Virus (HIV) and their study revealed that the cTp-e interval, Tp-e/QT and Tp-e/QTc ratios were prolonged and correlated to the severity of the disease in HIV-infected patients. Previous studies have revealed that the Tp–e interval, the Tpeak-Tend interval (Tpe), the interval from the T-wave peak to the end of the T wave, has been related to arrhythmogenesis, is specified as an index of totaldispersion of repolarization[2]. Prolonged Tp–e interval is predictable for ventricular arrhythmias and mortality [3]. Unal et al. showed that HIV-infected patients receiving combination antiretroviral therapy (cART) were associated withlonger Tp–e interval and Tp–e/QTc ratio and correlated positively with the duration of disease and the electrophysiologicalabnormalities, and negatively with CD4 count[4]. There were no informations about medical status of patients with HIV, duration of the disease and why hsCRP is higher in patients’ group. The patients were in active phases of infection. We think that these are important datas for results of the study. We thank the authors for adding this article to the literature

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Induction of Autophagy to Achieve a Human Immunodeficiency Virus Type 1 Cure

Cells ◽

10.3390/cells10071798 ◽

2021 ◽

Vol 10 (7) ◽

pp. 1798

Author(s):

Grant R. Campbell ◽

Stephen A. Spector

Keyword(s):

Human Immunodeficiency Virus ◽

Antiretroviral Therapy ◽

Human Immunodeficiency Virus Type ◽

Virus Type ◽

Functional Cure ◽

Immunodeficiency Virus ◽

Latently Infected ◽

Infected Cells ◽

Hiv 1

Effective antiretroviral therapy has led to significant human immunodeficiency virus type 1 (HIV-1) suppression and improvement in immune function. However, the persistence of integrated proviral DNA in latently infected reservoir cells, which drive viral rebound post-interruption of antiretroviral therapy, remains the major roadblock to a cure. Therefore, the targeted elimination or permanent silencing of this latently infected reservoir is a major focus of HIV-1 research. The most studied approach in the development of a cure is the activation of HIV-1 expression to expose latently infected cells for immune clearance while inducing HIV-1 cytotoxicity—the “kick and kill” approach. However, the complex and highly heterogeneous nature of the latent reservoir, combined with the failure of clinical trials to reduce the reservoir size casts doubt on the feasibility of this approach. This concern that total elimination of HIV-1 from the body may not be possible has led to increased emphasis on a “functional cure” where the virus remains but is unable to reactivate which presents the challenge of permanently silencing transcription of HIV-1 for prolonged drug-free remission—a “block and lock” approach. In this review, we discuss the interaction of HIV-1 and autophagy, and the exploitation of autophagy to kill selectively HIV-1 latently infected cells as part of a cure strategy. The cure strategy proposed has the advantage of significantly decreasing the size of the HIV-1 reservoir that can contribute to a functional cure and when optimised has the potential to eradicate completely HIV-1.

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