Before you go any further I recommend checking these blogs to get a crash course on how our immune system works. However if you wanna be a rebel then get stuck in. However if you are of the impatient type then you can jump to this section.
As of today (17th June 2020), 8,351,427 Covid-19 cases have been confirmed, resulting in 449,027 fatalities as per data from ‘Johns Hopkins University’, worldwide. After its discovery last December, in Wuhan, China, the virus started to spread around the world, causing panic. Interestingly though, there are over 200 types of corona-viruses of which only 7 affect humans. In these seven types, four of them are what causes 15-30% of the world’s common cold cases, two (SARS and MERS) of them are considered an epidemic and the seventh one is SARS-CoV-2 (Virus) or in other words COVID-19 (Disease). COVID-19 is not the first severe respiratory disease outbreak caused by the corona-virus. Just in the past two decades alone, corona viruses have caused three epidemic diseases, namely, COVID-19, Severe Acute Respiratory Syndrome (SARS) and Middle East Respiratory Syndrome (MERS). The occurrence and development of SARS-CoV-2 depend on the interaction between the virus and the individual’s immune system.
The impact depends on an individual’s immune response and for 80-85% of people infected by COVID-19, these symptoms will run their course much as they would with a case of the flu.
How do viruses work?
Imagine a virus as a memory stick with a certain program on it. Memory stick on its own is neither alive nor can it function by itself. It needs a system for its program to be executed. In a similar fashion, a virus is not really alive (or maybe its in a state of suspended animation), trapped in a perpetual state of 'Bardo' and yet it has an in-built program, which once downloaded into a host cell, it re-programmes it to make copies of itself, working as a template to replicate more viruses inside the body. Rather sneaky and sinister eh, not to mention it makes us ponder what it is to be really alive but that's for another blog!
There are more viruses than stars in the universe. So why do only some infect us?
There are enough viruses to assign, to each star in the universe 100 million times over. Seriously, we are surrounded and bathed in these viruses and yet we pretty much are left unscathed and relatively free of an illness. The reason for this lies more to do with the extraordinary fastidiousness of the viruses rather than our resilience to them. Nevertheless Covid-19 supposedly seems to be on a rampage with no sign of slowing down. So what gives?
For a virus to make a successful transition from one species to another, they have to go through something called a spillover event for which they have to jump through a lot of biological hoops. So its no wonder most of these transitions fizzle out and hardly leave a dent on us. As discussed in the Immunity blogs, for a pathogen or in this case a virus to do its job, it needs to gain access to our cells, which contain the molecular machinery that these pathogens need to replicate. In order to latch onto the receptors on our cells, first they need to get past our first line of defense, our physical barriers, then fight off our innate and adaptive immune system and somehow manage to latch onto a specific receptor, in this case ACE2, more on this a bit later. So these viruses most of the time pretty much die an unceremonious death (for good), leaving a part of them as a memento so the next time any of their cousins decides to avenge their loss, our body knows exactly how to deal with them and raise hell on them even before they can get started!
However viruses although supposedly not alive, somehow manage to beat our defenses and adapt to use human cell receptors. Although our immune system has evolved as well to be able to control many pathogens, pathogens themselves have evolved ways to evade the immune response. One such method of immune evasion is mutation, wherein they hijack our RNA as opposed to our DNA. This gives rise to a huge number of mutations as its a sloppy process leading to a staggering amount of mutations thereby enabling them to a wider diversity and adapt to new challenges.
They also work with their cousins who are vying for a slice of the same human cells, by exchanging information in form of segments of their genomes and turning hybrid in the process enabling them to make a stronger assault on our cells.
Genetic recombination is the combining of gene segments from two different pathogens is an efficient form of immune evasion. For example, the influenza virus contains gene segments
that can recombine when two different viruses infect the same cell. Recombination between
human and pig influenza viruses led to the 2009 H1N1 swine flu outbreak.
They also manage to stay under the radar, patiently waiting for an opportune moment to make an assault on us like when we are immune-compromised during winters etc. This is the reason why seasonal influenza viruses, for example, circulate globally every year, causing illness in tens of millions of people worldwide; WHO estimates that 290,000 to nearly 650,000 people die from seasonal influenza each year.
*Because influenza surveillance does not capture all cases of flu that occur in the U.S., CDC provides these estimated ranges to better reflect the larger burden of influenza.
Because viruses’ surface molecules mutate continuously, viruses like influenza change enough each year that the flu vaccine for one year may not protect against the flu common to the next.
New vaccine formulations must be derived for each flu season.
Disease Transmission
Transmission of infectious diseases can occur via a number of distinct mechanisms:
Direct contact: Transfer of pathogens via physical association or the exchange of body fluids
Contamination: Ingestion of pathogens growing on, or in, edible food sources
Airborne: Certain pathogens can be transferred in the air via coughing and sneezing
Vectors: Intermediary organisms that transfer pathogens without developing disease symptoms themselves
Pathophysiology of Covid-19
Coronavirus Disease 2019 (COVID-19), named after the Severe Acute Respiratory Syndrome Coronavirus-2 (SARS-CoV-2) due to its similarity and common origin to SARS-CoV, which caused acute respiratory distress syndrome (ARDS) and high mortality during 2002–2003, started as a zoonotic (animal to human) transmission associated with the seafood market in Wuhan, China. Later it was recognized that human to human transmission played a major role in the subsequent outbreak. SARS-CoV-2 seems to primarily affect the respiratory system, although other organs seem to be involved.
The life cycle of the virus with the host consists of the following 5 steps:
Attachment
Once the SARS-CoV-2 virus manage to get past the physical barriers and enter the lungs, they use their spike proteins (key), which look like a crown and hence 'Corona’, to Angiotensin-Converting Enzyme 2 (ACE2) receptor (Lock) of the host cell to gain entry. These receptors are mostly found in the respiratory tract. ACE2 expression is usually high in the lungs and is needed for the virus to gain entry into the lung cells, in this case it’s the Alveoli (cells where gas exchange takes place). These receptors are also present in heart, ileum, kidneys and bladder. In the lungs, ACE2 is highly expressed on the lung epithelial cells.
Angiotensin-converting enzyme is an important component of blood pressure regulation!
Entry
Ones it binds to the ACE 2 receptor it activates it and enters the cell through a process called endocytosis or through direct fusion of the viral envelope with the host membrane.
Biosynthesis
Once inside the cell It starts unpacking its RNA and fuses with the host cell's Ribosome. Endoplasmic Reticulum of the host cell will read these small strands of RNA, make structural components of the protein and sends it off to Golgi Apparatus.
Replication
Once synthesized, Golgi Apparatus packages it and they start replicating and new viral particles are made.
Release
The replicated new viruses are released outside of the cell through exocytosis to infect other cells.
So how exactly does our immune system deal with this virus and why does it seem to impact only a certain segment of the population? That's next.
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