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Group: Group VI (ssRNA-RT)
The Tyrant virus (also known as the Clay virus ε-strain) was the general designation for artificially improved variants of the Progenitor virus designed by the Umbrella Corporation for military use in the manufacture of living biological weapons known as "B.O.W. (Bio Organic Weapons)." It had mutagenic properties able to rapidly transform organisms and grant new capabilities impossible in the evolution of the natural world.
Countless strains existed ranging from the first primitive strain developed by James Marcus and the mass-produced strain perfected by William Birkin, while many independent strains were developed by other researchers in facilities around the world. The initial strain was unsuitable to create a practical B.O.W., but this fault was resolved over several decades of development. However, various experiments were repeated prior to completion and resulted in many failures. 1 2
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On December 4, 1966, an expedition team led by aristocrats Oswell E. Spencer, Edward Ashford and biochemist James Marcus, an authority on virology, discovered an ancient RNA retrovirus within a rare flower species in an underground cave system in West Africa. This discovery was inspired by a passage in the Natural History Conspectus by Henry Travis that described a ritual performed by the Ndipaya tribe involving the ingestion of the flower to gain superhuman capabilities.
Marcus hypothesized that these capabilities were caused by a virus rewriting the host's DNA upon ingestion. This hypothesis was confirmed following the discovery; the virus possessed the ability to recombine the genes of infected organisms due to a unique DNA mutation property. Spencer immediately formed an ambition based on this property and ordered the construction of a secret underground laboratory beneath his mansion in the Raccoon Forest region of the American Midwestern Arklay Mountains.
"Arklay Laboratory" was completed in November 1967 and populated by virologists, biochemists and molecular biologists hired by Spencer. Preliminary examination of the Progenitor virus discovered that it was extremely fatal to the majority of humans. From the outset, Spencer sought to use the virus as a tool to evolve mankind and create a new world populated by a superhuman species, with himself as "God." However, the virus' fatal nature made this plan impossible. In order to remedy this, Spencer formulated a research project to create a variant strain of the virus more adaptable to humans.
t-Virus Project (1967-1978)
On November 17, 1967, three of Spencer's researchers proposed another plan that could monopolize the military industry by changing the very concept of war. They thought of applying the mutagenic property of the Progenitor virus to develop a new form of biological weapon named "B.O.W. (Bio Organic Weapon)." These weapons would create an extraordinary new market in the military industry with high commercial viability. However, the research was still in a fundamental stage and long-term study was necessary to make the virus suitable for B.O.W. production. 3
Spencer approved the biological weapons plan and presented it to his collaborators. Edward Ashford began research on the Progenitor virus with his son Alexander Ashford and laid the foundation of the project with initial research to achieve the commercial viability of the Progenitor virus as a viral weapon through development of an improved variant strain. These variants were henceforth named "Tyrant" and the project became known as the "t-Virus Project." In order to camouflage and fund this research, Spencer founded a viral treatment pharmaceutical company in March 1968 with Ashford, Marcus and several other collaborators.
The t-Virus Project had three vital stages, the creation of the t-virus; the stabilization of the t-virus; and B.O.W. production. The project was the primary focus of Umbrella, with those who produced the best results wielding the most power within the company. Marcus and his student Brandon Bailey hit a wall in their research due to the inability to culture the Progenitor virus outside of its natural habitat, while Alexander Ashford gave up virus research and turned to genetic engineering. He formulated the "CODE:Veronica Project" in order to create a highly intelligent clone of his ancestor Veronica Ashford, who could succeed his father Edward's research and advance development of the t-virus.
In July, Edward Ashford died following infection with the Progenitor virus caused by an accident orchestrated by Spencer. As a result, the Ashford family quickly fell behind in t-virus research under Alexander's leadership and the family's influence within Umbrella quickly declined. 4
On September 19, 1977, Marcus conducted a Progenitor virus administration experiment with leeches. After much selective breeding, he discovered that the virus favorably recombined within the leeches, creating a new strain capable of keeping a host alive in a clinically dead state. The leeches showed signs of rapid mutation and gained intellect and mimicry abilities as a result of infection, sparking a fascination with them in Marcus as a potential B.O.W. host. Leech DNA also harbored properties favorable to the development of a biological weapon, including genes for nerve regeneration and metabolic attributes that allow a leech to survive in the absence of oxygen and subsist on its own dead tissue. 5
In October 1977, Marcus used the recombined virus to conduct administration experiments with insects, amphibians and mammals in order to narrow down efficient test subjects. Marcus was angered when these experiments failed to achieve results but noticed that mammals reached the most satisfactory degree of perfection and presented the most potential due to their intelligence, then deduced that further development of the virus couldn't be expected without using humans as the mammalian host. He began using company employees and junior executive candidates as test subjects, reaching about twenty victims. 6 7
On January 13, 1978, Marcus completed development of the t-virus through human testing that led to the creation of the humanoid B.O.W. "Zombie", made possible through the properties within the leech DNA he had incorporated. He planned to perfect a B.O.W. and present it to Umbrella Headquarters in order to upstage Spencer, through which he could grasp more power, regain his status as an Umbrella founder and cement his position as the company's top scientist. However, Spencer ordered the only two people Marcus trusted to steal a sample of the new virus, his students William Birkin and Albert Wesker.
On July 29, Spencer closed the training facility and promoted Wesker and Birkin as chief scientists in charge of the t-Virus Project in the Arklay Laboratory. Research on the virus progressed by leaps and bounds at the Arklay Laboratory while Marcus continued his own research in the abandoned training facility, during which time he created the frog-based Lurker, monkey-based Eliminator and hybrid insect-based Plague Crawler.
In the same year, the t-virus stolen from Marcus was transported to the Beardsley family's laboratory on Gadiwall Island to undergo research and development. Although there was some progress, an accident occurred and the virus accidentally leaked and infected many of the islanders, desolating the island.
Second Stage (1978-1981)
On July 31, 1978, Wesker and Birkin arrived at the Arklay Laboratory as chief researchers in charge of the facility's t-Virus Project. Spencer supplied an immense budget and many personnel to advance the project and used subtle manipulation to influence the two chiefs to succeed. After reviewing the potential of the recently discovered Ebola virus, Birkin improved the DNA mutation property of the t-virus by incorporating Ebola genes, increasing the effectiveness of the t-virus to 90% of humans.
Since gene manipulation could be performed easily on organisms with primitive body structures, research using insects was actively conducted with the virus in the initial stage of the Arklay Laboratory's project. One of these experiments produced the spider-based Web Spinner. The virus recombined favorably within the subject's body and produced a prototype known as the "α-strain." Several improved strains were subsequently created from the prototype through recombination within various living organisms in an effort to stabilize the virus.
In 1981, it became clear that due to delicate genetic differences between each human, the virus had a compatibility issue that meant even though the virus was effective against 90% of humans, the remaining 10% would remain unaffected. However, Spencer desired an independent weapon with 100% effectiveness. Eventually, the researchers extracted a new βI-strain able to create the dog-based Cerberus. Sometime after, they created the stabilized βII-strain and successfully reached the project's second stage.
As the virus also had the ability to make gene synthesis between different species comparatively easy, genetic combination between two or more living things was frequently conducted during the second stage through incorporating not only the t-virus' genetic manipulation, but also the genetic information of other creatures. By combining the characteristics each individual creature possessed, hybrid creatures with superior abilities could be created. The combination of creatures of different species groups at the gene level was naturally unstable, but they were supported by the t-virus' promotion of abnormal evolution, enabling higher forms of life.
One genetic hybrid devised by Birkin was a combination of human and reptile DNA to create a combat-focused B.O.W. capable of exterminating humans who escaped onset of infection or possessed anti-virus weapons and equipment, later known as the Hunter. Another hybrid B.O.W. was created by combining human and fly DNA, known as Chimera.
Third Stage (1988-1998)
In 1988, as the Arklay Laboratory's t-Virus Project had entered the third stage, a motion to stop Marcus' research became active as he was now unnecessary. Spencer ordered Wesker and Birkin to assassinate him and steal his research, which they then used to assist their own. Based on the results of various research findings, the Arklay Laboratory began development of a more advanced combat-focused B.O.W. Birkin proposed the "Tyrant Project", the conception of an ultimate life-form compliant with commands, considered to be the project's final goal and named after the virus that would create it.
Although the t-virus had the ground-breaking property to instantly evolve a creature, practicality was initially regarded as questionable since creatures were unable to endure the dramatic physical changes and often died. Due to this effect, research had reached a dead-end. As a way out, a method was devised to use an adult male with physical strength and immune system resistance as the host. However, although the βII-strain for producing Zombies and Hunters was adaptable for almost all humans, the virus' side-effect or necrosis considerably decayed brain tissue and subjects could not become a Tyrant without maintaining some intelligence.
In order to overcome the project's problem, Birkin extracted a new variant which suppressed influence on the brain to a minimum if it completely adapted. However, there were extremely few humans who could adapt to this variant. In order for research to progress and develop a new strain which would allow more humans to become Tyrants, a human with full adaptation to this variant was needed. Despite gathering test subjects close to the ideal genetic pattern by force from other laboratories, the project was left at a standstill for three years. 8
While the Tyrant Project was at a standstill, Albert Wesker was interested by the "Nemesis" parasite developed by the Umbrella Europe Sixth Laboratory, and convinced Birkin to administer the prototype of the parasite into the Arklay Laboratory's primary t-virus test subject, Lisa Trevor. However, an unexpected result occured when her body absorbed the parasite shortly after it reached her brain. Although initially baffled by this result, Birkin disregarded all prior data on Trevor and conducted a thorough examination, at which point he discovered that Trevor's genes harbored a vastly recombined t-virus. This new virus was extracted, and Birkin studied it over the next three years.
In 1991, Birkin recognized that the virus extracted from Trevor held potential surpassing that of the t-virus. He formulated the "G-Virus Project", a further development of the t-virus, and gained the approval of Spencer who was deeply interested in the new virus' potential to finally realize his ambition. Birkin was temporarily transferred to the underground laboratory beneath the secret France branch of Umbrella while construction began on a similar laboratory of massive scale beneath Raccoon City. Meanwhile, Albert Wesker left his position as a researcher and transferred to the Umbrella Intelligence Division.
As the t-Virus Project progressed, other sections of Umbrella proposed the virus' usage as a oncolytic viral treatment against cancerous diseases. In February 1991, a strain of the t-virus designed for this purpose was sold to the South American drug lord Javier Hidalgo as a treatment against the cancerous disease that afflicted his wife, Hilda Hidalgo. Over two months, Hilda's stamina was considerably restored. However, by May, she had yet to regain consciousness and her vitality surpassed that of a human. The continued injections of the virus eventually led her to mutate into an amphibious creature dramatically different from common human mutations. 9
In December 1991, former Soviet colonel Sergei Vladimir approached Umbrella looking for work and underwent a host adaptability test. The results of this test revealed that Vladimir's genome was compatible with the Arklay Laboratory's latest t-virus strain, which would allow him to become a Tyrant. Rather than waste a test subject so valuable, Spencer offered him an executive position within the company in exchange for allowing ten clones of himself to be created for Tyrant development. Vladimir accepted and research on the Tyrant Project progressed using these ten clones, with Birkin creating the new ε-strain which allowed more humans to become Tyrants.
In 1993, Birkin transferred to the Raccoon City underground laboratory. Elsewhere in the company, another oncolytic strain was designed and supplied to the private hospital in the Arklay Mountains. As with the case of Hilda two years prior, initial injection of the virus showed promising results by eradicating cancerous cells. However, the first test subject Doug Frost died due to a sudden change in condition. The second subject Dorothy Lester fully recovered, but the virus continued to spread within her body and eventually transformed her into a Zombie, leading to a brutal incident in which many staff and patients were killed. 10
In 1994, a scientist from Umbrella's Chicago branch was transferred to the Arklay Laboratory to replace Birkin as chief scientist, John Clemens. Within the next four years, the female spy Ada Wong infiltrated the Arklay Laboratory posing as a researcher and became Clemens' girlfriend, using him to obtain information on the t-virus which she leaked to a rival company. Meanwhile, the t-virus and G-virus projects advanced concurrently within the company with no superiority between them.
On May 11, 1998, the Tyrant (T-002 Type) was completed. However, an accident occurred during injection of the virus into the host, causing an airborne leak of the ε-strain within the Arklay Laboratory that infected the researchers and then contaminated the facility's water supply, exposing the above-ground employees. The accident was caused by the "Queen Leech", an intelligent mimicry of James Marcus.
A new mutant strain arose soon after the accident which exhibited the process "V-ACT" (Virus Activation). William Birkin secured the ε-strain, the V-ACT mutant strain and the Tyrant embryo to continue research. He created the enhanced Tyrant (T-103 Type) and used the mutant strain to develop an enhanced strain capable of creating a new creature, "Licker", then supplied the finalized virus for mass-production. This completed strain of the virus was subsequently supplied to Umbrella research facilities around the world in order to promote further development of new B.O.W. models. At the same time, the company began to develop functional antibodies and vaccines.
In June, Birkin feared he would be held responsible for the accident in the Arklay Laboratory that led to the leak of sensitive data on the company's biological weapons program. He expected the company to send agents to kill him and seize the G-virus, and so purposefully began to spread the t-virus in the sewers of Raccoon City and Umbrella's incineration disposal plant as a means to cut-off access to his underground laboratory. On July 23, the Queen Leech contaminated the Ecliptic Express with the primitive strain of the virus. To prevent the truth about Marcus from being exposed, Birkin destroyed the facilities.
On July 25, Albert Wesker stole the ε-strain and provided it to Umbrella's rival company with a vast quantity of B.O.W. combat data, allowing the company to begin their own virus and B.O.W. development.
On September 23, a large-scale leak of the t-virus occurred in the city sewers after an attack on William Birkin by the U.S.S. (Umbrella Security Service), sparking a city-wide outbreak that deteriorated into chaos and eventually complete desolation. Under the pretense of preventing the virus from spreading beyond the city, the American government launched the Sterilization Operation and wiped the city off the face of the earth in an attempt to eradicate evidence of their own involvement with the virus.
Umbrella researcher Frederic Downing was able to steal the t-virus and G-virus and escape Raccoon City prior to its destruction. He then erased his past and joined the WilPharma Corporation to lead development of a vaccine against the t-virus using his already intimate knowledge of the virus. While developing the vaccine, he thought about orchestrating a demonstration to prove its efficiency and prevent it from being sold other than as a combined set of both virus and vaccine.
An enhanced strain of the t-virus was developed on Gadiwall Island under the direction of Mylene Beardsley, an executive of Umbrella and 17th head of the Beardsley family. This strain was named the Neo t-virus and was lost due to a succession of incidents on the island. On December 27, the mass-produced t-virus leaked on Rockfort Island after an attack by the special operations unit HCF (Hive/Host Capture Force) belonging to Umbrella's rival company. Planes carrying this strain also crashed and caused another leak in the Umbrella Antarctic Base.
After the 1999 collapse of Umbrella U.S.A., further t-virus development was led by Umbrella Europe. It became apparent that due to the incomplete nature of the G-virus, its application towards B.O.W. development could not be expected. However, rather than scrap the virus, it was instead applied to a hybridization development project to merge it with the mass-produced strain of the t-virus. The favorable attributes of each virus were exchanged in order to remove each of their biggest faults, including intelligence degradation and volatile mutation. This project led to the creation of the t+G-virus.
Types of t-Virus
In the virus classification of the Umbrella Corporation, "t-Virus" refers to the original Progenitor virus and any of its variants. "Clay Virus" is a name synonymous with both the t-virus and Progenitor virus, with different researchers applying the "t" moniker at different stages.
- Progenitor Virus
- Progenitor Virus TYPE-A
- Progenitor Virus TYPE-B
- t-Marcus (Progenitor Virus + Leech DNA)
- t-Ebola (t-Marcus + Ebola genes)
- Clay Virus α-Strain
- Clay Virus βI-Strain
- Clay Virus βII-Strain
- Clay Virus T-Strain (first Tyrant creation strain)
- Clay Virus ε-Strain
- V-ACT Strain (mutation of ε-strain)
- t-Birkin (mass-production strain; improvement of V-ACT mutant strain)
Structure and Genome
The t-virus is roughly spherical in structure with a genome identical to the Progenitor virus, altered over several decades through the inclusion of new genes and repeated recombination.
In 1978, favorable mutation of the virus within a leech inspired James Marcus to incorporate leech DNA into the virus, containing genes that coded for nerve regeneration and metabolic processes that improved the virus' regenerative ability and allowed hosts to remain alive even in a clinically dead state. In 1981, William Birkin incorporated two immuno-suppressant genes from the highly pathogenic Zaire ebolavirus; VP24 and VP35.
Signs and Symptoms
Many of the virus' symptoms are not directly caused by the virus, but by the response of the immune system. After detecting the virus, the body produces a superantigen in order to combat infection. However, the strength of this superantigen eventually causes side-effects, such as fever. These symptoms eventually lead to the host's death with a prevailing fever and tachycardia (excessive heart rate), consistent with superantigenic toxic shock and elevated metabolism.
The virus damages the brain due to excessive replication as viral budding consumes minute quantities of the cell membrane, and if enough virions bud off of a cell, they can kill it. This widespread effect on brain cells leads to a dramatic decline in intelligence and motor functions. The exact level of damage varies between hosts even of the same species and limiting replication within the brain was key to maintaining the intelligence of a host.
The t-virus has a variety of transmission methods but is actually a naturally airborne virus, able to mutate into a form that spreads via direct skin contact (percutaneously). Infected hosts are immediately able to spread the virus via bodily fluids such as saliva through bites, but the virus also evolves over time due to the external environment, gradually growing into a more stable form which, after infecting and replicating within a host organism, transforms into a variant that spreads through the skin. It can be said that the t-virus is a virus strain that gradually grows less infectious over time. Although virtually any creature is a potential host and vector for the virus, insects and rodents pose the biggest threat due to their small size and huge numbers.
Hosts with a genome possessing B cells (lymphocytus B) that produce a rare natural antibody effective against the Progenitor virus are capable of adapting to the t-virus, although the effects are uncertain due to the rarity of this antibody and have only been displayed in connection with an experimental variant strain separate from Umbrella's mass-produced strain.
In initial exposure in animals, the virus attaches to the receptor protein, phospholipid, a molecular structure on the cell membrane that a virus must attach to in order to enter the cell's cytoplasm. Phospholipids are used by every cell in the human body and most animals, allowing the virus to successfully infect a wide-range of animals of varying species. In plants, the virus is able to enter the host's cytoplasm directly since they lack phospholipids.
Once inside the host cell cytoplasm, the virus uses its own reverse transcriptase enzyme to produce DNA from its RNA genome. This new DNA is then incorporated into the host cell genome by an integrase enzyme, at which point the retroviral DNA is referred to as a provirus. The host cell then treats the viral DNA as part of its own genome, translating and transcribing the viral genes along with the cell's own genes, producing the proteins required to assemble new copies of the virus.
VP24 (membrane-associated protein) prevents the establishment of cellular antiviral state by blocking IFN-α/β and IFN-γ signaling pathways by inhibiting the IFN-induced nuclear accumulation of host tyrosine-phosphorylated STAT1 through interaction with the STAT1-binding region of the host KPNA1 (karyopherin alpha 1/importin alpha 5) protein, inhibiting the latter. Without the activity of this protein, activated STAT1 is unable to enter the cell nucleus and cannot activate IFN-induced genes.
VP35 (polymerase complex protein) acts as a polymerase cofactor in the RNA polymerase transcription and replication complex and prevents establishment of a cellular antiviral state through interaction with the double-stranded RNA-binding protein PACT, which functions as a cellular activator of RIG-I (retinoic acid-inducible gene 1) to facilitate innate antiviral response, thereby blocking virus-induced phosphorylation and activation of interferon regulatory factor 3 (IRF3), a transcription factor critical for the induction of interferon's alpha and beta (IFN-α/β). This inhibits the antiviral state mediated by the double-stranded RNA-activated protein kinase EIF2AK2/PKR.
Interferon antiviral system evasion allows the virus to replicate optimally, spreading at a rate faster than the original Progenitor virus. The faster the virus spreads, the more dramatic and pronounced its effects with the additional benefit of increasing expression of the "Zombie" mutation at a success rate of approximately 90% in human hosts. After successfully taking up residence within the host's cells without rejection, the virus self-propagates using the synthesis properties and energy of proteins. In other words, the protein and nucleic acid synthesis program of cells infected with the t-virus are rewritten based on the nucleus of the virus, resulting in growing numbers of new t-virus nuclei. The virus replicates within the body spreading to its various systems, starting with the internal secretory systems.
The most common and noticeable sign of t-virus infection is a basic mutation referred to as "Zombie." This effect itself affects a wide range of host species and is comprised of several other side-effects with a significant degree of predictability and little variation. Immediately before transformation begins, the host undergoes fever and tachycardia induced by superantigenic toxic shock. Hosts infected through other methods and killed are technically not dead, as the virus has already begun to spread within their bodies, keeping them alive. The virus does not literally revive the dead, but it does prevent death.
After first spreading to the internal secretory systems, the virus stimulates the production of telomerase to limit telomere degradation caused by cellular division, giving hosts an increased natural lifespan. It also increases the secretion of growth hormone by up-regulating production of the hormone ghrelin, which is known to increase feelings of hunger. At the same time, it activates the host's metabolism through up-regulation of several other hormones, increasing effectiveness but at the cost of a stronger desire and necessity for food. The virus then spreads to nearly all organs constituting the body, such as the skin, muscles and nervous, circulatory, respiratory, digestive and skeletal systems.
The t-virus preferentially targets the skin and tissues of the outer integument for replication unless otherwise directly exposed to core tissues. As a result, the most immediate effect of the virus is necrosis of the skin, similar to the Progenitor virus. However, the causes and severity slightly differ between the two viruses. While necrosis caused by the onset of a superantigen is still prevalent in the t-virus, the effect is more dramatic due to an infected individual beginning to actively consume its own proteins as a source of energy, an effect derived from leech DNA.
The leech DNA in the virus includes early-activating genes that code for enzymes in the leech's metabolic processes such as various amino acid deaminase enzymes, as well as genes for hormones that up-regulate these processes. When these genes are expressed in a host, those enzymes and hormones allow host cells to continue energy production even as circulation shuts down and cells run out of oxygen. Cells continue to obtain nutrients from the lysate of dead cells and tissue surrounding them. This primarily included protein, which leeches naturally degrade as an energy source even in the absence of oxygen. This incidentally speeds up decomposition and further increases the need for hosts to consume animal tissue, almost completely eliminating herbivorous diets.
Infected cells produce ammonia while breaking down dead cell proteins for energy, helping to reduce acidity produced by increased glycolysis. The continued acquisition of nutrients and the ability to function in the absence of oxygen drastically reduces the importance of the heart, lungs and circulatory system. Not only can a host function with these organs operating at a reduced level, they can keep going even if these organs are severely damaged. These reactions create the common "Zombie" mutation. A human grievously injured by a Zombie can rise as one themselves, and a Zombie can continue to seek prey despite otherwise devastating injuries. This allows the virus to keep the host alive long enough to infect others.
The t-virus induces an overall strengthening effect within a host's muscles with the latent capabilities of the Progenitor virus, but its necrosis deteriorates actual muscle fibers. This limits the potential muscular enhancement of a host, but they still gain a significant increase in strength. Muscular necrosis can also be circumvented through artificial manipulation.
The t-virus is capable of an activation effect in response to external stimuli, such as physical trauma or starvation. When the host body suffers from these, an effect known as "V-ACT" (Virus Activation) occurs during which the host body enters a dormant state and undergoes a regenerative transformation stimulated by SAPK (stress-activated protein kinase) pathways, mechanisms used by cells to survive trauma such as starvation and heat shock. These pathways in turn stimulate the host cells rewritten by the t-virus to secrete hormones that trigger cellular growth throughout the body, leading to systemic transformation.
The leech DNA incorporated into the virus also included genes related to increased expression of matrix substrate molecules like laminin and tenascin; a process able to regenerate damaged nerves. In the case of an infected human host, this process repairs segments of the brain and recovers a certain level of motor coordination destroyed earlier during infection. This over-expression leads to the reestablishment of epiphyseal plates on the surfaces of some long bones in areas not occupied by ligaments, tendons, cartilage, or synovial fluid.
The most promising locations for this growth are the tips of the third-row phalanges. Bone growth in these areas leads to the development of what appear to be claws emerging from the skin of the fingers and toes, a secondary effect of overall metabolic and growth factor up-regulation. Rapid reestablishment of metabolism and repair of the heart restores blood pressure, leading to excessive blood seepage through the ruined arterioles and capillaries of the skin. The damaged lungs are reactivated and oxygenate the blood, giving it a bright red coloration.
The two mutations known to be created by this process are the Crimson Head created by a mutant strain and the Licker created by the mass-produced strain. The effects on the Crimson Head end here, but the Licker displays a further, significant enhancement of the process. The osteoblasts (bone-forming cells) of the new growth regions in the phalanges migrate over the surface of the metacarpals and metatarsals, and the hands and feet grow into enormous talons. Increased expression of proteins and hormones linked to muscle mass levels causes the host's muscles to tear through the skin and become completely exposed, with the intrinsic muscle of the tongue experiencing the most dramatic growth.
As osteoclasts (bone cells associated with absorption and removal of bone) eat away at the cranial dome, new brain tissue begins to grow, spurred by increased expression of the leech genes which regulate nerve regeneration. This gives the Licker some level of increased intelligence, but at the cost of the eyes as that part of the skull is degraded due to the brain's expansion. This nerve development also causes the growth of new follicle cells in the cochlea, giving the Licker a more sophisticated sense of hearing, which may or may not be compounded by potential natural compensation for the loss of sight.
The length of time between infection and transformation depends on countless factors. On a host level, these can include genetic compatibility, strength of the immune system, unrelated medication, resistance due to prior exposure and other indeterminable properties. On the virus level, these can include mode of transmission, amount of dosage, environmental resistance and the properties of the individual strain. As such, the virus' incubation period is wildly erratic and can range from mere minutes to several weeks. In some cases, the length of time can be used to deduce the mode of transmission, with secondary exposure generally taking longer.
The t-virus is capable of random antigenic variation as a means to circumvent the immune system and infect hosts that have already been infected, similar to other RNA viruses such as HIV-1 and the Influenza virus. This variation can be prompted by several factors, such as cross-species recombination and environmental changes.
- 1. biohazard archives (Page 299, 338)
- 2. BIOHAZARD archives II (Page 247)
- 3. Trevor's Notes (Trevor's Note 3 - November 17th)
- 4. Alexander's Memoir
- 5. Marcus' Diary 1
- 6. Report on B.O.W.
- 7. Marcus' Diary 1
- 8. Wesker's Report "Tyrant Project Problem"
- 9. Javier's Memorandum Book (1991)
- 10. Clinical Test Report