Hypothesis: Enveloped virus families bind specific receptor families.

Hypothesis title:
Enveloped virus families bind specific receptor families.

Abstract:
Enveloped viruses are known to use receptors to trigger endocytosis into host cells.  Looking at the infection patterns of virus families, there exists a corresponding receptor family.  As the viral key mutates over time the receptor it uses slightly changes but only slightly.  The mutated new virus tends to stay within the receptor family.  If we understand the homology of receptors and their tissue expression patterns, the new virus' receptor choice should be to some degree predictable. The goal of this paper is to establish the virus families with their corresponding receptor families.

Introduction:
Vaccines prepare the immune system for viral infections. Current viral drugs attempt to inhibit viral replication.  This hypothesis supplies another avenue for defeating viral infections. If we know what receptors the viruses are using we can anticipate and slow the viral infection of host cells by competing for those receptors.

There are 4 major enveloped viral families we can immediately see this pattern with: flaviviruses, herpes viruses, flu viruses, and human papilloma viruses.  If you look at the infection patterns of these viral families it becomes clear that the herpes viruses use estrogen receptors, flaviviruses use melanocortin receptors, flu viruses use dopamine receptors, and human papilloma viruses use cannabinoid receptors.

Even more striking is that if you assume that a virus within it's virus family has an ideal receptor that it uses as an entry point into a host cell you can deduce which specific receptor this virus is using based on the symptoms of the illness caused by the virus.

The flavivirus family for example if it uses the melanocortin receptors appear to have this simple pattern:

mcr1   Tick borne encephalitis virus/ hepatitis C  (Thrombocytopenia due to red blood cells with mcr1)

mcr2 (ACTH receptor)   Zika (placenta, developing brain)

mcr3  West nile (kidneys)

mcr3 and mcr1  Japanese encephalitis

mcr4  Yellow fever (liver)
                     
mcr5  Dengue (immune system T cells)

The reactivation of herpes viruses seem to be affected by estrogen.  There are 3 types of herpes viruses which if you look at where they infect match up with the types of estrogen receptors.

Alpha-herpes viruses: Herpes simplex 1, herpes simplex 2,  herpes zoster : Estrogen-beta receptors (nerves and uterine tissue )

Beta-herpes viruses: CMV, HHV6, HHV7 :  Estrogen-related receptors (CMV binding confirmed)

Gamma-herpes viruses: EBV, HHV8 : Estrogen-alpha receptors (lymphocytes, breast involved)

Flu viruses appear to use dopamine receptors:

Here is how the 5 types of dopamine receptors (D) that might match up with the A, B, and C flu viruses

D1 and D5 are similar but have reverse expression patterns.  D5 has the highest expression at birth then it decreases. D1 slowly increases in your life and is at it's lowest at birth.

D1 is the most abundant of the central nervous system. ( D1 and D5 )

D1 type B flu (encephalitis)

D5 type C flu (infects infants)

D2 is similar to D3 and D4.   D2 is expressed on the pancreas.

Type A flu and D2 receptors ( H1N1 and D3/D4 )

I am currently trying to elucidate other viral families. The receptor patterns have not been as obvious.

Enteroviruses (coxsackie, polio etc) may bind nicotine receptors
http://angelabiggs.blogspot.com/2016/08/enteroviruses-and-nicotine.html

The  Paramyxoviridae (measles family viruses) may bind the Muscarinic receptors 

http://angelabiggs.blogspot.com/2016/09/do-paramyxoviridae-measles-family.html