Spanish flu

INTRODUCTION:

Influenza typically referred to as the flu, is a viral disease that has been around for a long time. Descriptions of local outbreaks of what’s believed to be influenza date back to ancient times. However, the most famous influenza pandemic swept the world back between 1918 and 1919Even though this pandemic is commonly known as the “Spanish Flu,” this name is actually the result of a widespread misunderstanding, and experts can’t agree on precisely where it came from. What we do know is that about one-third of the world’s population became infected with this virus, and it’s estimated that at least 50 million people died worldwide.

Detail on Molecular Level Of Virus:

                   Let’s dig into the details of the virus on the molecular level;

Family Orthomyxoviridae.

In fact, Influenza A, B, and C viruses are the only members of the Orthomyxoviridae family. Since Influenza A causes the most serious disease, we’ll focus on the details of that one here.

Structure:

Influenza viruses themselves can be spherical or tubular in shape, ranging in diameter from Influenza A has eight segments of single-stranded RNA, which are enclosed in a protein capsid. The capsid is surrounded by a lipoprotein envelope that it gets from the host cell membrane during the maturation step of replication, and that lipoprotein has glycoprotein spikes poking out all around. The two glycoproteins that make up the spikes of the envelope are called hemagglutinin, abbreviated with the letter H, and neuraminidase, abbreviated with the letter N. The spikes are an important part of the virus's ability to cause damage, so we should try to understand why this is the case.

The hemagglutinin spikes allow the virus to recognize and then attach to specific receptors on host epithelial cells. Viruses that have these hemagglutinin spikes also cause red blood cells to stick together, which is called hemagglutination, and this is one method for identifying if a virus is present.

Neuraminidase is an enzyme that’s crucial for releasing newly formed virions from the host cell.

MODE OF INFECTION:

 Influenza viruses bud out of the host cell, taking some of the host’s lipoprotein envelope with it, but the newly formed virions need neuraminidase to break free from the surface receptors they were bound to. Neuraminidase destroys these receptors so that the virus can go on to infect another cell. And while we’re talking about this mechanism, anti-influenza drugs like Tamiflu act by inhibiting neuraminidase activity, which is why it’s important for these drugs to be taken very early in the infection cycle.

You’ve likely heard people talk about “H1N1” or “H5N1” influenza viruses, but what does that actually mean?

TYPES OF "INFLUENZA VIRUS A" :

Influenza A viruses can be split into subtypes based on what kinds of hemagglutinin and neuraminidase spikes they have.

These subtypes are given numbers, so H1, H2, N1, N2, and so on.

There are 16 H and 9 N subtypes total, but only H1, H2, and H3, as well as N1 and N2,

are spread amongst humans. The “avian flu” that got passed around back in 1997 was caused by the influenza virus H5N1, while the “swine flu” epidemic of 2009 was caused by the influenza virus H1N1.

MECHANISM:

Influenza typically enters a host by inhaling aerosolized respiratory secretions. So basically, little sneeze or cough droplets, from a person who has the flu. However, you can also pick up the flu virus from commonly-touched surfaces such as doorknobs or household items. In this case, the person touches something with the virus on it and then accidentally touches their face, transferring the virus into the mucous membranes of the face via the nose or eyes. The virus then attaches, using its hemagglutinin spikes, to respiratory epithelial cells coated in cilia, and uses the process of endocytosis to enter the cell. From there, the virus replicates its RNA and builds more of its own proteins using the host cell’s machinery. Within six hours, mature virions bud out of the host cell, taking some of the host cell’s membrane with them, and the virus then can spread rapidly to nearby cells.

 

In most cases, a small percentage of people with influenza die, but when outbreaks are widespread, that means the number of people who are likely to die goes up. And actually, most of the deaths that occur from influenza outbreaks are from secondary bacterial infections like pneumonia.

 

Epidemics of influenza happen each year, but global pandemics only pop up periodically. The reason for this really boils down to the mutation and evolution of the virus. First, there’s the concept of antigenic drift, which is important for Influenza A and B viruses.

Basically, point mutations in the genes that encode the hemagglutinin and neuraminidase spikes, causing a single amino acid discrepancy during normal viral replication, for instance, can grant the virus the ability to escape the immune system.

In other words, one single mutation might weaken the interaction of the virus with antibodies that we’ve already made against them. Antigenic drift commonly occurs during the course of a standard flu season.

In some cases, enough changes accumulate in a virus that a new subtype evolves. A more uncommon occurrence is the idea of antigenic shift. Only influenza A viruses can do this because it requires the swapping of genetic material between different subtypes of the same kind of virus. Remember when we talked about the genome of the influenza virus is segmented, meaning that viral protein is encoded in eight separate segments?

If someone is infected with two different subtypes of Influenza A at the same time, so that both viruses are replicating within the same cell, it’s possible for a newly created virus to contain pieces of each of the subtypes. While this is rare, it’s absolutely possible, and this is the way that viruses are able to “jump” to infect new species.

This viral genome reassortment is what causes pandemic influenza. Now let’s talk about treatment and prevention. Since influenza is a virus, antibiotics don’t work to treat the infection. Some antiviral medications can prevent disease if taken early, but the main form of prevention is the vaccine. Since these viruses are prone to continual evolution, it is very difficult to create a vaccine that offers lifelong immunity. Because of antigenic drift, a slightly new strain of influenza is always emerging, and it typically takes between 6 and 9 months to manufacture large quantities of a vaccine once a new strain emerges.

However, scientists are working to develop a universal flu vaccine that could revolutionize 


influenza prevention, which would neutralize a major killer worldwide.



 

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