In the latter case, the suitable host species tend to be taxonomically related, sharing similar morphology and physiology.
The early isolated infection events exposes the pathogen to the selection pressure of survival in that new species of which some will eventually adapt to.
This gives raise to pathogens with the primary adaptations allowing the smaller outbreaks within this potential new host, increasing exposure and driving further evolution.
Sufficiently adapted pathogens may also reach pandemic status meaning the disease has infected the whole country or spread around the world.
Humans infected from the bite of rabid animals do not tend to pass on the disease and so are classed as dead-end hosts.
The following pathogens are examples of diseases that have crossed the species barrier into the human population and highlight the complexity of the switch.
Influenza - also known as the flu - is one of the most well-known viruses that continues to pose a huge burden on today's health care systems and is the most common cause of human respiratory infections.
These host switch events create pandemic strains that eventually transition into seasonal flu that annually circulates in the human population in colder months.
The RNA polymerase enzyme of influenza has low level accuracy due to a lack of a proofreading mechanism and therefore has a high error rate in terms of genetic replication.
[10] Because of this, influenza has the capacity to mutate frequently dependent of the current selection pressures and has the capability to adapt to surviving in different host species.
These proteins recognise sialic acid that reside on the terminal regions of external glycoproteins on host cell membranes.
However, HA proteins have different specificities for isomers of sialic acid depending on which species the IAV is adapted for.
The influenza genome is replicated using the virus RNA-dependent RNA polymerase but it must adapt to use host specific cofactors in order to function.
[10] Specifically, residue 627 of the PB2 unit shows to play a defining role in the host switch from avian to human adapted influenza strains.
[13] The cellular protein ANP32A has been shown to account for contrasting levels of avian influenza interaction efficiency with different host species.
However, when that mammalian cell contains the avian ANP32A protein, viral replication is mostly restored,[15] showing that the ANP32A is likely to positively interact and optimise the polymerase action.
Mutations in the PB2 making the influenza mammal-adapted allow for the interaction between the viral polymerase and the mammalian ANP32A protein and therefore essential for the host switch.
HIV is the human immunodeficiency virus and attacks cells of the immune system depleting the body's defence against incoming pathogens.
[16] When HIV sufficiently diminishes the immune system, it causes a condition known as acquired immunodeficiency syndrome or AIDS characterised by severe weight loss, fever, swollen lymph nodes and susceptibility to other severe infections [17] HIV is a type of lentivirus of which two types are known to cause AIDS: HIV-1 and HIV-2,[16][18] both of which jumped into the human population from numerous cross-species transmission events by the equivalent disease in primates known as simian immunodeficiency virus (SIV).
Each type is proposed to have emerged through bush-meat hunting and the exposure to the body fluids of infected primates,[18] including blood.
Host-specific selection pressures would bring about a change in the viral proteome of HIVs to suit the new host and therefore these regions would not be conserved when compared to SIVs.
This amino acid is conserved as a methionine in SIVs but mutated to an arginine or lysine in HIV-1 groups M, N and O,[18][19] suggesting a strong selection pressure in the new host.
[19] This is evidence of the reason behind the mutation (optimal levels of replication in host CD4+ T lymphocytes), however the exact function and action of the position 30 amino acid is unknown.
[21] This incomplete cytoplasmic domain renders Nef proteins found in SIVs ineffective as an anti-tetherin response in humans and so in order to switch from non-human primates to a human host, the SIV must activate the Vpu protein which instead blocks tetherin through interaction with the conserved transmembrane region.