Sharing CD4+ T Cell Loss: When COVID-19 and HIV Collide on Immune System

Abstract

COVID-19 is a distinctive infection characterized by elevated inter-human transmission and presenting from absence of symptoms to severe cytokine storm that can lead to dismal prognosis. Like for HIV, lymphopenia and drastic reduction of CD4+ T cell counts in COVID-19 patients have been linked with poor clinical outcome. As CD4+ T cells play a critical role in orchestrating responses against viral infections, important lessons can be drawn by comparing T cell response in COVID-19 and in HIV infection and by studying HIV-infected patients who became infected by SARS-CoV-2. We critically reviewed host characteristics and hyper-inflammatory response in these two viral infections to have a better insight on the large difference in clinical outcome in persons being infected by SARS-CoV-2. The better understanding of mechanism of T cell dysfunction will contribute to the development of targeted therapy against severe COVID-19 and will help to rationally design vaccine involving T cell response for the long-term control of viral infection.

Immune characteristics of human immunodeficiency virus/severe acute respiratory syndrome coronavirus 2 coinfection: A case report and mini-review

“…The rate of decline from CD4 is relatively large, gradually increasing in distance from CD8, which eventually leads to the inversion of the ratio of CD4/CD8; therefore, early HIV infection mainly causes damage of CD4. According to Xiaorong Peng, 12 when COVID-19 and HIV collide on the immune system, they share CD4 losses. For the HIV/SARS-CoV-2 coinfection patient, in line with our clinical observations, early anti-coronavirus treatment was given with general or specific compassionate drug use, from day 1 to day 12; CD8 decreased rapidly, from the second week to the fourth week of onset; and CD4 and CD8 reached a plateau period.…”

Mecanismos subyacentes a la linfopenia en la infección por SARS CoV-2, y su relación con la severidad de la enfermedad.

“…A pesar de que las personas en su mayoría cursan con cuadros asintomáticos o con síntomas leves (5), una fracción de los pacientes puede desarrollar un cuadro severo con un síndrome inflamatorio sistémico similar a otros virus de la misma familia como el SARS-CoV y el MERS-CoV (síndrome respiratorio de medio oriente), con elevación de distintas citoquinas e interleucinas (IL-6, TNF, IL-1, IL-2, IL-17, IFN--y G-CSF (6).…”

Lymphopenia, Lymphopenia-Induced Proliferation, and Autoimmunity

“…Infections may mediate LIP by several ways. First, lymphopenia is frequently associated with many viral infections, such as influenza virus [ 190 , 191 ], measles virus [ 192 ], rubella virus [ 193 ], parvovirus [ 194 ], HIV [ 195 ], and SARS-CoV-2 [ 149 ]. Second, activation of autoreactive T cells can be mediated by infections with bacteria or viruses through the following mechanisms [ 196 ]: (i) molecular mimicry, (ii) bystander activation after tissue damage caused by proinflammatory cytokines (such as TNF-α) which are released from antigen-presenting cells (APCs) after stimulation of Toll-like receptors (TLRs) and other pattern-recognition receptors (PRRs) [ 141 ], and (iii) epitope spreading to other autoreactive B cells after more tissue destruction by activated autoreactive T cells and inflammatory cytokines [ 196 ].…”