COVID-19 vaccine and boosted immunity: Nothing ad interim to do?

Abstract

Today, Coronavirus Disease 2019 (COVID-19) is a global public health emergency and vaccination measures to counter its diffusion are deemed necessary. Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the etiological agent of the disease, unleashes a T-helper 2 immune response in those patients requiring intensive care. Here, we illustrate the immunological mechanism to train the immune system towards a more effective and less symptomatic T-helper 1 immune response, to be exploited against SARS-CoV-2.

Keywords: Bacillus Calmette-Guérin (BCG); Coronavirus Disease 2019 (COVID-19); Corynebacterium parvum (C. parvum); Cutibacterium acnes (C. acnes); Hyaluronic acid; Propionibacterium acnes (P. acnes); Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2); T helper 1 (T(h)1); T helper 2 (T(h)2); Vaccine; cluster of differentiation 44 (CD44).

Fig. 1

Illustrative clinical photographs taken by Prof. Palmieri before and after C. parvum vaccination: herpes zoster of the scalp pre-injection (A) and 48 h post-vaccine (B); herpes labialis before the injection (C) and after 24 h from the treatment (D); genital herpes at the time of subdermal injection (E) and 24 h post-vaccination (F).

Fig. 2

Illustrative scheme of our vaccination rationale: following SARS-CoV-2 entry (point 1), the immune system is forced to mount a T_h2 response in those patients requiring intensive care, at the expense of a more effective and less symptomatic T_h1 response, compromised by the viral load (point 2). Through C. parvum or BCG vaccine (point 3), it is theoretically possible to train and calibrate the immune system towards a T_h1 response (point 4), able to prevent COVID-19 or to keep the disease under control in a paucisymptomatic or asymptomatic way thanks to activated reticuloendothelial system, NK, T_c and dendritic cells.