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The beastie of Doom |
Introduction
This
post is a brief introduction to some aspects of the coronavirus.
Clearly, within the limitation of the blogging format, the topic
under consideration can only dealt with in a superficial manner: this
is not a learned scientific treatise.
The
pathogen responsible for the disease COVID-19 (as stated by the World
Health Organisation) is designated as a severe acute respiratory
syndrome coronavirus 2 (SAR-CoV-2). This is quite a mouthful of
nomenclature but entirely warranted considering the mayhem and chaos
the virus is currently causing. The genome of SAR-CoV-2 has been sequenced and
the virus has been classified as a betacorona virus with filial
affinity to the virus responsible for severe respiratory syndrome
(SARS). The virus also has a genetic affiliation to several bat
coronaviruses. This relationship has led some workers to consider
that a bat coronavirus is ultimately responsible for the outbreak. It is envisaged, therefore, that an
initial mutation in the bat virus allowed the virus to leap the species barrier thus enabling the infection of a human host.
The
virus was first detected in late December 2019 as the cause of a cluster of pneumonia infections in patients from Wuhan city, China.
The disease spread quickly throughout China and soon thereafter
became disseminated across the globe. SAR-CoV-2 is mainly spread by
nasal droplets expelled when infected individuals cough and sneeze.
Thus individuals coming in contact with airborne viral particles or
viral particles having settled on surfaces can become infected. The
time of contact to the expression of symptoms varies between patients
but a mean incubation period of 4 days has been reported.
The
clinical presentation of the condition is variable in regard to
symptoms and severity. The majority of individuals appear to have
relatively mild symptoms (about 80%) and severe illness is more
prevalent in the elderly and those with already underlying health
problems such as pulmonary and cardiac disease.
In
general, the symptoms can be described as ‘flu-like’. Thus
patients may complain of a dry cough, fever, aching muscles, and
fatigue. The most serious manifestation of the condition is
pneumonia. The overall fatality rate has been estimated at about 2.3% however, a high level of variance between countries has been reported. The reason
for the mortality variance is complex and often poorly understood.
Countries with an ageing population (eg Italy) have experienced
relatively high death rates of 7%. Indeed it is suspected that
reported death rates are inflated as a consequence of ascertainment
bias.
With
that said, let's have a look at the virus itself.
First
off, I’ll not get bogged down with scientific semantics/pedantics
concerning the moot point whether viral particles actually constitute
life.
Coronaviruses,
unlike the vast majority of organisms, do not rely on DNA for genome
replication. Instead, they utilise a related molecule called
RNA, in a single strand format. The virus is characteristically
globular in structure and sports a series of protein protrusions on
the surface. These ‘spiky’ projections give the virus its name as
corona translates to ‘crown’ in Latin. Specific viral proteins
present on the spikes seek out and attach to specific and
complementary receptor proteins on the host cell. The ACE2 receptors
are uniquely present on cells that form the lower and upper
respiratory tract and this ‘key and lock’ association facilitates viral entry into the cell. Once ensconced, the virus,
like all viral particles, uses its limited genome to hijack the host cell's
protein and nucleic acid making apparatus. In this way, numerous viral
particles are formed and assembled within the host cell. Once the assembly has been completed, the newly manufactured viral particles are
released and ready to infect new cells within the host or expelled
into an awaiting and expectant outside environment: thus disseminated
the infection cycle continues anew.
A
particular characteristic of RNA viruses is their high mutation rate
as they lack the proofreading capacity and necessary nucleic acid repair
mechanisms of higher organisms and even DNA based viruses. This is a
headache for researchers hoping to produce an effective vaccine as
new mutations may circumvent and hence negate a targeted vaccine.
The US, as are other nations, are currently undertaking trials to test novel vaccines. The introduction of a new vaccine tends to be
exceedingly and excruciatingly slow due to the painstaking protocol
inherent in the introduction of any new therapeutic agent. This is
crucially important as not only the efficacy of the agent need to be
evaluated but also the risk of undesirable side effects requires assessment. Even if a vaccine proves promising, general availability
and widespread distribution are unlikely to occur for at least a year.
Unlike other viral vaccines, the vaccine currently under
investigation does not utilise a deactivated or attenuated virus
particle. Instead, the vaccine is an artificial laboratory
constructed piece of messenger RNA (mRNA). Messenger RNA is a crucial
intermediary in the production of proteins. The presence of this
particular mRNA induces cells to manufacture a protein found on the
outer surface of the virus and the presence of this protein
stimulates the host immune system to manufacture a repertoire of
antibodies. These antibodies are expected to attach to the outer coat
of the virus, if encountered, thereby inducing the host's immune machinery
to lock on and neutralise this grievous offender. Well, that’s the
theory at least, whether this works in practice awaits further
elucidation and research.
A
different approach is being considered and applied. There are a number
of drugs, already evaluated, that have been shown to induce a viral
limiting response, either in prophylaxis or during active infection.
These drugs have the advantage that they have already been evaluated
for efficacy and side effects and thus they can be introduced after
limited evaluation. The downside: there are a number of drugs of this
ilk that need to be specifically assessed for SAR-CoV-2. This will
take a little time but because of the number of agencies working on
the issue, I’m sure the research can be fast-tracked. That said,
unless we find a ‘wonder’ viral agent, the results are unlikely
to be as effective as a specific vaccine.
Enough
science for now as I’ve just overrun the critical 1,000-word limit
for a blog. Unwritten as the rule may be, it is one that the prudent
blogger must adhere to, otherwise, astute readers will bugger off to
more succinct pastures.
However,
I’m tempted to continue writing upon the fertile field of COVID-19.
There is much to cover, such as social impact, epidemiology, etc,
etc. If readers would like me to wax lyrical on other aspects of the
disease, I’m more than willing to comply/apply. Tis good for my
mental health, apparently. Just let me know in the comments. Arse.