The human host evolved a number of strategies to prevent microbial infection.
As we know, hosts evolved a number of defense systems in response to the challenge from parasites.
In this regard, African trypanosomes have evolved an array of host evasion mechanisms, including the phenomenon of antigenic variation of the variable surface glycoprotein (VSG) to successfully inhabit the extracellular space, as in the case with T. congolense, in full view of the host immune system [ 5- 7].
However, the cardiac kernel is likely to have evolved in the context of a host of ancient TFs controlling ubiquitous cellular processes such as metabolism, cell cycle, chromatin dynamics, and cytoskeleton.
While hosts have evolved a variety of mechanisms to recognize and counter pathogens, the rare combinations leading to disease cause significant damage to the host.
As the concept started to evolve, it became associated with a host of other midlife problems, such as relationship woes, trouble with adolescent kids, career despair and -- most notably -- the irrepressible need to buy a red sports car.
Wolbachia is typically maternally inherited through the egg cytoplasm and has evolved a variety of interactions with its hosts, exerting subtle effects such as manipulation of host reproduction or protection against natural enemies [ 4- 6].
Unfortunately, in our case, it was not possible to perform RT-PCR for detection of CHIKV in synovial fluid or tissue Viruses have evolved a number of mechanisms for suppressing host immune responses.
Accordingly, hosts have evolved a great variety of defence mechanisms to prevent all sorts of exploitative attacks [ 3, 4].
Subject to RNA‐based adaptive immune responses in their hosts, viruses have evolved a variety of genes encoding proteins capable of suppressing the immune response.
