Emergence and molecular mechanisms of SARS-CoV-2 and HIV to target host cells and potential therapeutics

Abstract

The emergence of a new coronavirus, in around late December 2019 which had first been reported in Wuhan, China has now developed into a massive threat to global public health. The World Health Organization (WHO) has named the disease caused by the virus as COVID-19 and the virus which is the culprit was renamed from the initial novel respiratory 2019 coronavirus to SARS-CoV-2. The person-to-person transmission of this virus is ongoing despite drastic public health mitigation measures such as social distancing and movement restrictions implemented in most countries. Understanding the source of such an infectious pathogen is crucial to develop a means of avoiding transmission and further to develop therapeutic drugs and vaccines. To identify the etiological source of a novel human pathogen is a dynamic process that needs comprehensive and extensive scientific validations, such as observed in the Middle East respiratory syndrome (MERS), severe acute respiratory syndrome (SARS), and human immunodeficiency virus (HIV) cases. In this context, this review is devoted to understanding the taxonomic characteristics of SARS-CoV-2 and HIV. Herein, we discuss the emergence and molecular mechanisms of both viral infections. Nevertheless, no vaccine or therapeutic drug is yet to be approved for the treatment of SARS-CoV-2, although it is highly likely that new effective medications that target the virus specifically will take years to establish. Therefore, this review reflects the latest repurpose of existing antiviral therapeutic drug choices available to combat SARS-CoV-2.

Keywords: COVID-19; HIV; Molecular mechanisms; Origin and taxonomy; Potential therapeutics.

Fig. 1

Schematic illustration of the virion morphology of coronavirus (a) and HIV (b).

Fig. 2

The general genome structure of Coronaviridae shared across the family, consisting of a positive-sense ssRNA genome of 27–32 kb in size. Starting from the 5′-terminal with approximately two-thirds of the genome encoding for polyprotein, pp1ab, which is cleaved into 16 non-structural proteins that are involved in genome transcription and replication. The 3′-terminal end possesses the primary structural genes encoding for ‘spike’ (S) protein, envelope (E) protein, membrane (M) protein and nucleocapsid (N) protein.

Fig. 3

Comparison of various coronavirus members of their respective genera: NL63 associated with lower respiratory tract disease, Rhinolophus bat coronavirus HKU2, Human coronavirus OC43, HKU1 possessing the enzyme haemagglutinin-esterase, severe acute respiratory syndrome coronavirus (SARS-CoV) strain GD02, Bat (SARS)-like Virus KY417151, severe acute respiratory syndrome coronavirus (SARS-CoV-2) isolated from Wuhan in December 2019 Genbank Accession number: MN908947 (Wu et al. 2020), Middle East respiratory syndrome coronavirus (MERS-CoV), Bat coronavirus HKU 14–1, Bat coronavirus HKU9-1, Infectious bronchitis virus (IBV), Beluga whale coronavirus SW1, Bulbul coronavirus HKU11 and Sparrow coronavirus HKU17.

Fig. 4

Comparison between various members of the Lentivirus genus reference genome. Human Immunodeficiency Virus 1 (HIV1), Human Immunodeficiency Virus 2 (HIV2), Simian Immunodeficiency Virus (SIV) and Feline Immunodeficiency Virus (FIV).

Fig. 5

Crosstalk of the infection mechanism and cell death of COVID-19 and HIV.

Fig. 6

Chemical structure of (a) chloroquine and (b) remdesivir.