I decided to look up meningitis (swelling of the brain, I found it is closely related with Encephalitis) after watching a documentary about a neuroscientist that got it and went into a coma and had a near death experience which he cannot explain through his science.
Symptoms include headache, fever, confusion, drowsiness, and fatigue. More advanced and serious symptoms include seizures or convulsions, tremors, hallucinations, and memory problems.
It turned out it can be caused by bacteria and viruses. And of course there are lots of flavors and colors of viruses that cause it.
The most common causes of viral encephalitis are Rabies, Herpies Simplex, Polio, SSPE and PML. Other causes include infection by flaviviruses such as St. Louis encephalitis or West Nile virus, or by Togaviridae such as Eastern equine encephalitis (EEE), Western equine encephalitis (WEE) or Venezuelan equine encephalitis (VEE).
Other viruses involved: Enteroviruses, Arbovirus, Mumps, Herpes family viruses, Lymphocytic choriomeningitis virus (arenaviruses), Adenovirus, Measles (Morbillivirus), Varicella zoster virus, Rabies, HIV, H5N1 encephalitis, Lymphocytic choriomeningitis.
So I centered on the FLAVIVIRUSES:
Flaviviruses are named from the yellow fever virus, flavus means yellow in latin
size: 40-65 nm
symetry: enveloped, icosahedral nucleocapsid
RNA: 10k-11k bases. Positive-sense, single stranded.
Bite from an infected arthropod (mosquito or tick). Human infections with these viruses are typically incidental, as humans are unable to replicate the virus to high enough titres to reinfect arthropods and thus continue the virus life cycle.
The exceptions to this are yellow fever and dengue viruses, which still require mosquito vectors, but are well adapted to humans to not depend upon animal hosts (although both continue have important animal transmission routes as well).
Other virus transmission routes include handling infected animal carcasses, blood transfusion, child birth and through consumption of unpasteurised milk products.
The transmission from animals to humans without an intermediate vector arthropod is thought to be unlikely. Test showed that the disease is not contagious.
The dengue viruses produce millions of infections annually due to transmission by a successful mosquito vector. As mosquito control has failed, several dengue vaccines are in varying stages of development.
yellow fever 17D vaccine, introduced in 1937.
A tetravalent chimeric vaccine that splices structural genes of the four dengue viruses onto a 17D yellow fever backbone is in Phase III clinical testing.
Effective killed (inactivated) Japanese encephalitis and Tick-borne encephalitis vaccines were introduced in the middle of the 20th century. Inactivated mouse brain-derived vaccine. Unacceptable adverse events have prompted change to safer and more effective second generation Japanese encephalitis vaccines, production ceased in 2005.
The Beijing-3 strain, inactivated vaccine cultivated on primary hamster kidney cells, used in the People’s Republic of China from 1968 until 2005.
Three second-generation vaccines have entered markets since then: SA14-14-2, IC51 and ChimeriVax-JE. The live-attenuated SA14-14-2 strain was introduced in China in 1988. It is cheaper than alternative vaccines, and is administered to 20 million Chinese children each year.
A purified, formalin-inactivated, wholevirus vaccine known as IC51 (marketed in Australia and New Zealand as JESPECT and elsewhere as IXIARO) was licensed for use in the United States, Australia, and Europe during the spring of 2009. It is based on a SA14-14-2 strain and cultivated in Vero cells ( Isolated cells from kidney epithelial cells extracted from an African green monkey).
Another vaccine, a live-attenuated yellow fever-Japanese encephalitis chimeric vaccine known as ChimeriVax-JE (marketed as IMOJEV) was licensed for use in Australia in August 2010
Is a vaccine created by reducing the virulence of a pathogen, but still keeping it viable (live). Attenuation takes an infectious agent and alters it so that it becomes harmless or less virulent. These vaccines contrast to those produced by “killing” the virus (inactivated vaccine).
Viruses may be attenuated via passage of the virus through a foreign host, such as:
The initial population is applied to the foreign host. One or more of these will possess a mutation that enables it to infect the new host. These mutations will spread, as the mutations allow the microorganisms to grow well in the new host. The result is a population that is significantly different to the initial population, and will not grow well in the original host when it is re-introduced to the original host (that is why it is “attenuated”).
This makes it easier for the host’s immune system to eliminate the agent and thus create the immunological memory cells which will likely protect the patient if they are infected with a similar version of the microorganism in “the wild”.
In the cytoplasm of the host cells.
The genome (+ sense RNA) mimics the cellular mRNA molecule in all aspects except for the absence of the poly-adenylated (poly-A) tail. This feature allows the virus to exploit cellular apparatus to synthesise both structural and non-structural proteins.
In general the genome encodes 3 structural proteins (Capsid, prM, and Envelope) and 8 non-structural proteins NS (NS1, NS2A, NS2B, NS3, NS4A, 2K, NS4B and NS5).
The genomic RNA is modified at the 5′ end of positive strand genomic RNA with a cap 1 structure (???)
Cellular RNA cap structures are formed via the action of an RNA triphosphatase, guanylyltransferase, N7-methyltransferase and 2′-O methyltransferase. (???)
The virus encodes these activities in its non structural proteins. The NS3 protein encodes a RNA triphosphatase within its helicase domain. It uses the helicase ATP hydrolysis site to remove the γ-phosphate from the 5′ end of the RNA. The N-terminal domain of the non structural protein 5 (NS5) has both the N7-methyltransferase and guanylyltransferase activities necessary for forming mature RNA cap structures. RNA binding affinity is reduced by the presence of ATP or GTP and enhanced by S-adenosyl methionine. This protein also encodes an 2′-O methyltransferase.
Once translated, the polyprotein is cleaved by a combination of viral and host proteases to release mature polypeptide products.
Cellular post-translational modification is dependent on the presence of a poly-A tail this makes the process not host-dependent. Instead, the polyprotein contains an autocatalytic feature which automatically releases the first peptide, a virus specific enzyme. This enzyme is then able to cleave the remaining polyprotein into the individual products. One of the products cleaved is a polymerase, responsible for the synthesis of a (-) sense RNA molecule. Consequently this molecule acts as the template for the synthesis of the genomic progeny RNA.
Flavivirus genomic RNA replication occurs on rough endoplasmic reticulum membranes in membranous compartments.
New viral particles are subsequently assembled. This occurs during the budding process which is also responsible for the accumulation of the envelope and cell lysis.