Journal of Clinical Respiratory Medicine

All submissions of the EM system will be redirected to Online Manuscript Submission System. Authors are requested to submit articles directly to Online Manuscript Submission System of respective journal.

Short Communication - Journal of Clinical Respiratory Medicine (2022) Volume 6, Issue 1

Impact and pathophysiology of covid-19 delta variant on lungs

Samuel Ivan*

Institute of Medical Immunology, Charité University Medicine, Berlin, Berlin, Germany

*Corresponding Author:
Samuel Ivan
Institute of Medical Immunology
Charité – University Medicine Berlin
Berlin
Germany
E-mail:
[email protected]

Received: 27-Jan-2022, Manuscript No. AAJCRM-22-101; Editor assigned: 29-Jan-2022, PreQC No. AAJCRM-22-101(PQ); Reviewed: 12-Feb-2022, QC No AAJCRM-22-101; Revised: 15-Feb-2022, Manuscript No. AAJCRM-22-101(R); Published: 22-Feb-2022, DOI:10.35841/aajcrm-6.1.101

Citation: Ivan S. Impact and pathophysiology of covid-19 delta variant on lungs. J Clin Resp Med. 2022;6(1):101

Visit for more related articles at Journal of Clinical Respiratory Medicine

Introduction

COVID-19 (Coronavirus illness 2019) has been shown to be a highly contagious and rapidly developing disease. The culprit was identified as severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a single-stranded RNA virus with a positive sense. Human angiotensin-converting enzyme 2 (hACE2) is used by the severe acute respiratory syndrome coronavirus 2 to enter cells, infecting the lungs, heart, and other important organs, and causing haematological abnormalities and organ deficits. Due to the shifting variations of SARS-CoV-2, the virus–host interaction may change to varying degrees. Simultaneously, the clinical features and pathogenic processes of the COVID-19 pandemic have been well-documented since it began [1].

Coronaviruses are positive-stranded RNA viruses that are enclosed. The coronavirus that causes COVID-19 is a betacoronavirus in the same subgenus as the severe acute respiratory syndrome (SARS) virus (as well as other bat coronaviruses), but in a distinct clade, according to full-genome sequencing and phylogenic analysis. The International Committee on Virus Taxonomy's Coronavirus Study Group has suggested that this virus be named severe acute respiratory syndrome coronavirus. (SARS-CoV-2). Another betacoronavirus, the Middle East respiratory sickness (MERS) virus, appears to be more distantly related. The two bat coronaviruses have the closest RNA sequence similarity, and it appears that bats are the major source; whether COVID-19 virus is transferred directly from bats or by some other route is unknown [2]. The angiotensin-converting enzyme 2 (ACE2) is the same host receptor for SARS-CoV-2 cell entrance as it is for SARS-CoV. The receptor-binding domain of SARS-spike CoV-2's protein interacts to ACE2. SARS-CoV-2 cell entrance appears to be aided by the cellular protease TMPRSS2.

In the ORF1 downstream areas, all coronaviruses have particular genes that encode proteins for viral replication, nucleocapsid production, and spike creation. The glycoprotein spikes on coronaviruses' outer surface are responsible for the virus's attachment and penetration into host cells. Because the virus's receptor-binding domain (RBD) is loosely linked, it can infect several hosts. SARS-CoV and MERS-CoV, on the other hand, identify exopeptidases as a critical receptor for entrance into human cells, whereas other coronaviruses prefer aminopeptidases or carbohydrates. A coronavirus's entrance method is dependent on cellular proteases such as human airway trypsin-like protease (HAT), cathepsins, and transmembrane protease serine 2 (TMPRSS2), which divide the spike protein and cause additional penetration modifications.

SARS-CoV-2 has the conventional coronavirus structure with spike protein and additionally expresses RNA polymerase, 3-chymotrypsin-like protease, papain-like protease, helicase, glycoprotein, and accessory proteins, among other polyproteins, nucleoproteins, and membrane proteins. To sustain van der Waals forces, the SARS-CoV-2 spike protein has a 3-D structure in the RBD region. The crucial lysine 31 residue on the human ACE2 receptor recognises the 394 glutamine residue in the RBD region of SARS-CoV-2 [3].

The orf1ab gene, which encodes the pp1ab protein and 15 nsps, is the biggest gene in SARS-CoV-2. The orf1a gene produces the pp1a protein, which has 10 nsps. SARS-CoV-2 is closely related to the group of SARS-coronaviruses, according to the evolutionary tree. Recent research has shown significant differences between SARS-CoV and SARS-CoV-2, including the lack of 8a protein and alterations in the amount of amino acids in the 8b and 3c proteins in SARSCoV-2. The Wuhan coronavirus Spike glycoprotein has also been discovered to be changed by homologous recombination. SARS-spike CoV-2's glycoprotein is a combination of bat SARS-CoV and an unknown Beta-CoV. It was shown in a fluorescence investigation that the SARS-CoV-2 employs the same ACE2 (angiotensin-converting enzyme 2) cell receptor and mechanism for entrance into the host cell as the SARS-CoV [4]. The single N501T mutation in SARS-Spike CoV-2's protein may have increased the virus's ACE2 binding affinity considerably.

Therapeutic strategies

To lower the viral load, interferon nebulization, broad-spectrum antibiotics, and antiviral medicines were first employed; however, only remdesivir has showed promise against the virus. SARS-CoV-2 replication was strongly inhibited by remdesivir alone or in combination with chloroquine or interferon beta, and patients were deemed clinically recovered. Other antivirals are now being tested in the fight against infection. When tested against infection in people and in vitro clinical isolates, Nafamostat, Nitazoxanide, Ribavirin, Penciclovir, Favipiravir, Ritonavir, AAK1, Baricitinib, and Arbidol showed modest results.

Several alternative combinations, such as mixing antivirals or antibiotics with traditional Chinese treatments, were also tested in people and rats to see if they might prevent SARSCoV- 2 infection. In recent investigations, doctors obtained blood plasma from COVID-19 patients who had recovered clinically and injected it into infected individuals who had favourable outcomes and recovered quickly. A monoclonal antibody (CR3022) was discovered to bind to the spike RBD of SARS-CoV-2 in a recent investigation. Because the antibody's epitope does not coincide with the divergent ACE2 receptor-binding motif, this is most likely the case. CR3022 has the potential to be developed as a therapeutic option for COVID-19 infection prevention and therapy, either alone or in combination with other neutralising antibodies [5].

Conclusion

The new coronavirus was discovered at a Hunan seafood market in Wuhan, China, where bats, snakes, raccoon dogs, palm civets, and other animals were traded, and it quickly spread to 109 countries. SARS-zoonotic CoV-2's origins is unknown, although sequence-based study suggests bats are the main reservoir. DNA recombination was discovered at the spike glycoprotein, which mixed SARS-CoV (CoVZXC21 or CoVZC45) with the RBD of another Beta CoV, perhaps explaining cross-species transmission and fast infection. SARS-CoV is related to SARS-like bat CoVs, according to phylogenetic trees. Until present, no effective therapeutic therapies or preventative measures for human coronaviruses have been established.

References

  1. Peiris J, Guan Y, Yuen K. Severe acute respiratory syndrome. Nat Med. 2004;10(12):S88-S97.
  2. Indexed at, Google scholar, Cross Ref

  3. Riou J, Althaus CL. Pattern of early human-to-human transmission of Wuhan 2019 novel coronavirus (2019-nCoV), December 2019 to January 2020. Euro Surveill. 2020;25(4): 2000058
  4. Indexed at, Google scholar, Cross Ref

  5. Zheng BJ, Guan Y, Wong KH, et al. SARS-related virus predating SARS outbreak, Hong Kong. Emerg Infect Dis. 2004;10(2):176.
  6. Indexed at, Google scholar, Cross Ref

  7. Shi Z, Hu Z. A review of studies on animal reservoirs of the SARS coronavirus. Virus Res. 2008;133(1):74-87.
  8. Indexed at, Google scholar, Cross Ref

  9. Huynh J, Li S, Yount B, et al. Evidence supporting a zoonotic origin of human coronavirus strain NL63. J Virol. 2012;86(23):12816-25.
  10. Indexed at, Google scholar, Cross Ref

 

Get the App