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DEAD ANCESTORS. "The exogenous viral counterparts of HERVs have most likely been extinct for many millions of years, but it is clear that these elements have expanded in copy number significantly throughout the course of primate evolution, perhaps through intracellular retrotransposition mechanisms." https://lnkd.in/eW3mbzE View in LinkedIn

PATTERN RECOGNITION RECEPTORS (PRRs) "include toll-like receptors (TLRs), nucleotide oligomerization domain (NOD) like receptors (NLRs), and retinoic acid-inducible gene I (RIG-I) like receptors (RLRs)." https://lnkd.in/eFuy4KS View in LinkedIn

DIVORCING ADAPTION. "By constantly replacing the amino acids encoded at just a few residue positions, TFR1 divorces adaptation to ever-changing viruses from preservation of key cellular functions. These dynamics have driven genetic divergence at the TFR1 locus that now enforces species-specific barriers to virus transmission, limiting both the cross-species and zoonotic transmission of these viruses." https://lnkd.in/eGuH7sA View in LinkedIn

TFR1, HOST HOUSEKEEPING GENE. "While infectious disease research has long focused on host antiviral proteins, host proteins that facilitate viral replication are now an exploding area of inquiry. Essential housekeeping genes like TFR1 successfully balance the opposing selective pressures exerted by host and virus...TFR1 evolution in rodents has been shaped by two separate host-virus arms races." https://lnkd.in/eGuH7sA View in LinkedIn

VIRAL ENTRY PORTAL. "Transferrin Receptor (TfR1) is the cell-surface receptor that regulates iron uptake into cells, a process that is fundamental to life. However, TfR1 also facilitates the cellular entry of multiple mammalian viruses." https://lnkd.in/eGuH7sA View in LinkedIn

HOST DEFENSES. "Cells respond to virus attack by activating a variety of signal transduction pathways leading to the production of interferons, which limit or eliminate the invading virus. The presence of viruses inside the cell is first sensed by pattern recognition receptors (PRRs) that recognize the pathogen associated molecular patterns (PAMPs)." https://lnkd.in/eFuy4KS View in LinkedIn

AGENTS OF CELL DEATH. "Depending upon the need, a virus may inhibit or induce apoptosis for the obvious purpose of replication and spread, respectively. Interference in mitochondrial function can cause either cell death due to deregulation of the Ca2+ signaling pathways and ATP depletion or apoptosis due to regulation of Bcl-2 family proteins. Apoptosis is a programmed cell death." https://lnkd.in/eFuy4KS View in LinkedIn

STRESS AND MITOCHONDRIA. "During stress conditions, a small fraction of electrons leave complex III and reach complex IV. This premature electron leakage to oxygen results in the formation of two types of superoxides, namely, in its anionic form, and in its protonated form." https://lnkd.in/eFuy4KS View in LinkedIn

TOXIC REACTIVE OXYGEN SPECIES (ROS). "The mitochondrial respiratory chain is the main and most significant source of reactive oxygen species (RO) in the cell. Superoxide is the primary ROS produced by mitochondria. In the normal state, there is little or no leakage of electrons between the complexes of the electron transport chain." https://lnkd.in/eFuy4KS View in LinkedIn

OXIDATIVE STRESS. "A number of viruses cause oxidative stress to the host cells, which directly or indirectly helps them to survive. Many viral proteins alter mitochondrial ion permeability and/or membrane potential for their survival in the cell." https://lnkd.in/eFuy4KS View in LinkedIn