SARS-CoV2

Spike Proteins

Research article: "Density estimation of SARS-CoV2 spike proteins using super pixels segmentation technique"[1]

Spike

Proteins

Proteins that are located on the surface of the virus.

Allow the virus to enter human host cells by binding to a protein on human host cells.

Main role in pathogenesis is to facilitate the virus’s entry into the host cell.

Non-structural Proteins

[2]

Non-structural Proteins

- Assist in virus replication and transcription.

- Interfere with essential host cell functions.

- NSP1 – downregulate translation of NKG2D-L ligand.

- NKG2D receptor not activated.

- No signal to NK cell to lyse infected cell.

Pathogenesis

- Little to no resistance to infected cell proliferation 48hrs after infection.

- Virus replicates and spreads easily around body worsening symptoms.

[2]

Lee et al. [Nsp1 reduces NK cell ligand signal production, leading to evasion apoptosis] [2]

RNA-dependent RNA-polyermase (RdRp)

[3]

RNA-dependant RNA-polymerase

(RdRp)

Research article:

“Structural Basis of Ribosomal Frameshifting during Translation of the SARS-CoV-2 RNA genome”

RdRp:

- viral enzyme synthesised by Ribosomal Frameshifting

Ribosomal frameshifting is caused by a abnormally shaped Hairpin loop sticking to the mRNA channel causing tension on mRNA.

RdRp Pathogenesis factors:

SARS-CoV-2 rapid replication results from:

- Enhancement of transcription of SARS-CoV-2 genome through RNA processing

[3]

Immune evastion Stratergies

Immune Evasion Stratergies

The SARS-CoV-2 virus has the intrinsic ability to impair the production of type 1 beta interferons through repression of mRNA translation.

Aids in pathogenesis by repressing mRNA translation of interferons, inhibiting innate immunity within hosts.

Non-structural protein 2 enhances interactions between GIGYF2 and 4EHP.

Conclusion and contributions:

Concluding statement

&

Contributions

Team contribution:

All team members contributed equally to the assessment task, as we all researched and sourced an original article on a particular virulence factor of SARS-CoV-2. Through utilising the research piece, we each articulated our own statements on how SARS-CoV-2 utilised these four virulence factors (spike proteins, non-structural proteins, RNA dependent RNA polymerase, immune envasion stratergies) to cause coronavirus and the role they had on pathogenesis.

Collaboratively, we all wrote an introduction and conclusion, as well as deciding on the structure, framework and layout of our assessment.

The production of the video was collaboratively agreed upon to be conducted on zoom, with an occupying prezi designed presentation, to capture the attention of our targeted audience. Each individual presented their own virulence factor and its effect on pathogenesis, therefore having equal amounts of presenting time.