Corona Virus: Q1: Coronavirus Life Cycle
Corona Virus: Q1: Coronavirus Life Cycle
QUESTIONS :
Q1: CoronaVirus Life Cycle
For virion replication to begin, the spike proteins first bind to specific host
cell surface receptors that are embedded in the host cell membrane - a
process called host cell recognition
In the case of SARS-CoV, this receptor is angiotensin-converting enzyme 2
(ACE2). ACE2 is a regular cellular protein that happens to be used by the
virus to gain entry to the cell. It has been confirmed that the new
coronavirus SARS-CoV-2 also binds to ACE-2 and structurally resembles
SARS-CoV.
Once the binding between the spike protein and the receptor is complete,
the virion enters the cell through one of two processes.
Membrane Fusion
membrane fusion from without where viral and cellular membranes fuse
and the RNA genome of the virus gets access to the cytosol. endocytosis
where the receptor-bound virus is enveloped by the cell membrane and
enters the cytosol within a vesicle.
Uncoating Of RNA
Following either route of cell entry, the viral RNA genome is released into
the cytoplasm which is followed by uncoating of the RNA
Replicase Gene
Translation
Production of RNA
These shorter mRNAs code for the structural proteins (e.g., S, E, M, and N)
and nonstructural accessory proteins, including the viral proteinases, during
translation.
Translocation
Maturation
Here the new virions assemble, start maturing, and bud off from the Golgi
membranes as vesicles. These vesicles are translocated to the host cell
membrane. where they fuse with the host cell membrane and are released
into extracellular space.
Exocytosis
This release process does not rupture the host cell and is called nonlytic
exocytosis
QUESTION 2
Why it's so hard to design vaccines for coronavirus
QUESTION 3
DIFFERENCE BETWEEN ANIMALS AND HUMANS CORONAVIRUS
ANIMALS CORONAVIRUS
Coronaviruses cause a large variety of diseases in animals, and their ability
to cause severe disease in livestock and companion animals such as pigs,
cows, chickens, dogs, and cats led to significant research on these viruses
in the last half of the twentieth century. For instance, Transmissible
Gastroenteritis Virus (TGEV) and Porcine Epidemic Diarrhea Virus (PEDV)
cause severe gastroenteritis in young piglets, leading to significant
morbidity, mortality, and ultimately economic losses. PEDV recently
emerged in North America for the first time, causing significant losses of
young piglets. Porcine hemagglutinating encephalomyelitis virus (PHEV)
mostly leads to enteric infection but has the ability to infect the nervous
system, causing encephalitis, vomiting, and wasting in pigs. Feline enteric
coronavirus (FCoV) causes a mild or asymptomatic infection in domestic
cats, but during persistent infection, mutation transforms the virus into a
highly virulent strain of FCoV, Feline Infectious Peritonitis Virus (FIPV), that
leads to development of a lethal disease called feline infectious peritonitis
(FIP). FIP has wet and dry forms, with similarities to the human disease,
sarcoidosis. FIPV is macrophage tropic and it is believed that it causes
aberrant cytokine and/or chemokine expression and lymphocyte depletion,
resulting in lethal disease.
HUMAN CORONAVIRUS