How COVID-19 Hijacks Human Immune System

Coronaviruses are named for the crown-like spikes on their surface. It constitutes the family coronaviridae. Coronaviruses are minute in size i.e. 65-125 nm in diameter and having single-stranded RNA as genetic material. The subgroups of the coronavirus family are alpha (α), beta (β), gamma (ƴ) and delta (Δ) coronavirus.

The SARS-CoV-2 (the novel coronavirus that causes coronavirus disease 2019, or COVID-19)

The virus that causes Covid-19 is currently spreading around the world. Also there are six other types of coronavirus are known to infect humans, with some causing the common cold and two causing outbreaks: Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS).

SARS-CoV-2 multiplication

• Entry of virus

The virus enters the body through the nose, mouth or nose, then attaches to cells in the airway that produce a protein called ACE-2.

• Releasing viral RNA

The virus infects the cell by fusing its oily membrane with the membrane of the cell. Once inside, the coronavirus releases a genetic material i.e. RNA.

• Hijacking the cell

Overtake the cellular machinery.

• Making viral proteins

As the infection progresses, the machinery of the cell begins to churn out new spikes and other proteins that will form more copies of the coronavirus.

• Assembling new copies

New copies of the virus are assembled and carried to the outer edges of the cell. 

• Spreading  the infection

Each infected cell can release millions of copies of the virus before the cell finally breaks down and dies. The viruses may infect nearby cells, or end up in droplets that escape the lungs. 

• Leaving the body

Coughing and sneezing can expel virus-laden droplets onto nearby people and surfaces, where the virus can remain infectious for several hours to several days. The people diagnosed with Covid-19 should wear masks to reduce the release of viruses. Health care workers and others who care for infected people should wear masks, too. 

The virus is enveloped in a bubble of oily lipid molecules, which falls apart in contact with soap. So the best way to avoid getting infected with the coronavirus is to wash your hands with soap.

Role of  host cell proteases in  the cellular entry of SARS-CoV

Adeline Heurich et al. J. Virol. 2014; doi:10.1128/JVI.02202-13

Host cell entry of SARS-CoV can proceed via two distinct routes, dependent on the availability of cellular proteases required for activation of SARS-S (spike glycoprotein). The first route is taken if no SARS-S-activating proteases are expressed at the cell surface. Upon binding of virion-associated SARS-S to Angiotensin-converting enzyme-2 (ACE2), the functional receptor of SARS-CoV-2, plays a crucial role in the infection of COVID-19, as it provides viral entry into human cells, virions are taken up into endosomes, where SARS-S is cleaved and activated by the pH-dependent cysteine protease cathepsin L. The second route of activation can be pursued if the SARS-S- protease type II transmembrane serine proteases (TMPRSS2) is coexpressed with ACE2 on the surface of target cells.  Binding to ACE2 and processing by TMPRSS2 are believed to allow fusion at the cell surface or upon uptake into cellular vesicles but before transport of virions into host cell endosomes. Uptake can be enhanced upon SARS-S activation of metalloprotease ADAM17, which cleaves ACE2, resulting in shedding of ACE2 in culture supernatants. Since normal expression of ACE2 protects from lung injury and ACE2 levels are known to be reduced in SARS-CoV infection, the ADAM17-dependent ACE2 shedding is believed to promote lung pathogenesis. The present study suggests that the cellular uptake of SARS-CoV can also be augmented upon ACE2 cleavage by TMPRSS2. Since the entry-promoting function of ADAM17 is not undisputed and increased uptake upon ACE2 cleavage by TMPRSS2 has only been demonstrated with soluble SARS-S1, the respective arrows are shown in dashed lines.

COVID-19: consider cytokine syndromes and immunosuppression

Patients with severe coronavirus disease in 2019 (COVID-19) associated pneumonitis and/or acute respiratory distress syndrome.- increased pulmonary inflammation, thick mucous secretions in the airways, elevated levels of serum proinflammatory cytokines, extensive lung damage, micro thrombosis. Approx 10-15% of patients progress to acute respiratory distress syndrome (ARDS) triggered by a cytokine storm. Exacerbated and poorly understood host response involving a cytokine storm that drives severe COVID-19.

Neutrophil extracellular traps and COVID-19

Neutrophilia predicts poor outcomes in patients with COVID-19. The neutrophil-to-lymphocyte ratio is an independent risk factor to severe disease.

According to the research –

In COVID-19 patients- CD4 and CD8 T cell counts decrease, levels of TNF-α, IL-6 and IL-10 in ICU patients are significantly higher than in Non-ICU patients, CD19 B cell increases, Antibody Secreting Cells (ASC) increases, ASC of CD19+  B cells higher in extrafollicular-COVID, Translational of CD19+ B cells lower in extrafollicular-COVID.

How we say it’s HIJACKING