Unnamed Bio-Virus

The K5-63 virus—commonly referred to by humans as the “unnamed biovirus”—is a non-terrestrial, bioengineered agent of unknown origin, first encountered by human personnel during exploratory operations in the Tau3 Eridani System. At the time of discovery, the substance appeared inert and unthreatening: a dense, amorphous mass with no immediate pathogenic characteristics, presenting only minor reactive qualities in controlled lab environments. Initially classified as a low-risk xenobiological anomaly, it was collected, stored, and subjected to a battery of aggressive experimental manipulations—despite the absence of comprehensive genomic analysis or containment certainty.
It was this tampering, driven by curiosity and unchecked scientific ambition, that catalyzed the virus’s transformation from a passive, dormant construct into a catastrophic biological entity. Human researchers, unaware of the deeper architecture encoded within the substance, introduced mutagens, sequencing triggers, and metabolic accelerants in an attempt to “activate” its dormant functions. In doing so, they inadvertently unlocked a complex, adaptive system—one that responded not with data, but with evolution. What followed was not infection in the conventional sense, but systemic conversion. The once-stable biomatter became volatile, responsive, and self-replicating. It began interfacing with terrestrial life at a molecular level, overriding cell structures and reprogramming hosts to serve an emergent directive beyond human comprehension. The virus now functions as a vector of assimilation and reconstruction, capable of rewriting the physiology and neurology of any viable lifeform it contacts. It does not merely kill or feed—it transforms.
Officially, K5-63 is recognized as one of the most virulent and enigmatic biological threats ever encountered. Its ability to convert organic life into networked constructs, its immunity to all known treatments, and its capacity for silent, airborne spread have rendered it nearly impossible to contain once active. Its presence, once localized to a single containment breach, has now become a symbol of scientific hubris—a warning carved not into stone, but into the bones of the infected.
There is no cure. There was no understanding. There was only the first mistake—humanity’s belief that it could dissect something it was never meant to awaken.

The K5-63's life cycle

Infection

The K5-63 virus initiates infection upon direct contact with its primary substance—an amorphous, non-Newtonian bio-organic mass. Once in proximity to viable biological material, the virus exhibits an aggressive adhesion response, penetrating tissue barriers through biochemical osmosis and molecular mimicry. Host vulnerability increases in environments with high moisture content or elevated ambient temperature, as the virus demonstrates pronounced thermophilic and hydrophilic behavior.
Upon successful tissue penetration, the virus enters a latent integration phase, during which it remains undetectable by most immune systems. It exploits the host’s cellular machinery to replicate using a retroviral vector mechanism, incorporating fragments of its own synthetic genome into the host's DNA. This phase is characterized by silent systemic colonization—typically spanning one to three weeks—during which the host displays no observable symptoms. Following sufficient replication, the virus transitions into an active expression phase. Host biology is then gradually restructured via a cascade of epigenetic triggers, enzymatic rewrites, and targeted neurochemical modulation. In this stage, alterations begin at the microcellular level—first affecting the lymphatic and endocrine systems, then progressing to neuromuscular tissues and the central nervous system. These modifications are not externally visible in the early stages but prepare the host for full behavioral and morphological changes.
Secondary transmission becomes viable once internal viral saturation reaches critical mass. The K5-63 virus then undergoes spontaneous aerosolization within the host’s pulmonary system. This results in the continuous exhalation of microscopic viral spores, each capable of infecting new hosts via standard respiratory intake. Infection through fluidic transfer (blood, saliva) and dermal contact has also been confirmed, though at lower efficiency. Notably, the virus shows no selectivity regarding biological complexity. Although ostensibly engineered for unicellular biochemical modulation, it exhibits remarkable adaptability, proving lethal and transformative across a wide spectrum of multicellular lifeforms. This anomaly strongly suggests an evolutionary or artificial enhancement—whether through preexisting latent code or externally introduced mutation.
The infection process is irreversible without complete cellular destruction of the host. Even partial exposure to environmental inhibitors, radiation, or antiviral agents appears only to delay the transformation, not halt it. Hosts reaching full transformation often lose higher cognitive faculties, though some retain partial sentience—suggesting a spectrum of neurological outcomes that may relate to the virus’s emerging collective behavior observed in later stages.

Spread

The K5-63 virus demonstrates an exceptionally high transmission efficiency across a range of biological environments, with multiple redundant infection vectors that make containment challenging once initial exposure occurs. Following host saturation, the virus activates its aerosolized propagation phase, wherein infected individuals begin to exhale fine particulate spores composed of virion clusters suspended in protein-rich carriers. These airborne particulates are microscopic—measuring under 0.5 microns—and remain suspended in breathable air for extended periods under most atmospheric conditions.
Airborne spread is the primary vector, particularly in enclosed, humid, or poorly ventilated environments. The virus's bioengineered structure allows it to resist conventional filtration systems, and standard decontamination protocols are only partially effective. This airborne viability can persist even after the death of a host, as decomposing tissue continues to emit infectious particulates until fully neutralized by thermal or chemical sterilization. Secondary vectors include direct physical contact with infected biological matter—blood, saliva, sweat, or skin secretions—though these pathways exhibit lower infectivity rates than aerosol transmission. Even so, surface contamination remains a serious threat, as K5-63 displays unusual resistance to environmental degradation. On synthetic or organic surfaces, viable viral material has been recorded remaining infectious for up to 96 hours, particularly in warm, humid conditions. Tertiary transmission has been observed through fluid exchange between organisms, including bite wounds or open lesions. In such cases, infection appears nearly instantaneous, with no latency delay, suggesting a direct neurovascular bypass wherein the virus floods host tissues immediately upon entry. These aggressive transfer instances are less common, but disproportionately responsible for rapid cluster outbreaks—especially in high-density biological populations.
Notably, the virus demonstrates a form of adaptive intelligence in its dispersal patterns. Hosts in later stages of infection often exhibit behaviors that increase proximity to uninfected individuals, possibly driven by neural manipulation intended to maximize exposure. This pseudo-instinctive behavior is erratic but statistically significant across outbreak reports, suggesting that the virus not only spreads via passive mechanisms but may also exert subtle influence over host movement and interaction. K5-63’s propagation is further compounded by its incubation period. As most hosts remain asymptomatic for multiple weeks, infection frequently spreads unchecked across transport hubs, habitation modules, or shared life-support systems before detection protocols are activated. By the time symptomatic expression becomes visible, the virus typically has embedded itself across multiple population nodes. Due to its aggressive resilience and multi-modal transmission, containment of K5-63 requires complete atmospheric isolation, full biohazard quarantine, and sterilization protocols exceeding standard biosafety thresholds. Conventional antimicrobial measures are ineffective, and resistance to antiviral agents increases with each generation of viral replication, further complicating suppression efforts.

First Symptoms

The initial internal symptoms of K5-63 infection typically manifest after the viral latency period concludes, ranging from 10 to 24 days post-exposure depending on host physiology, immune efficiency, and environmental stressors. These symptoms mark the onset of the virus’s active expression phase, during which internal systems begin responding to progressive genetic and biochemical alterations.
The first and most consistent symptom is a deep, systemic fatigue that does not respond to rest, caused by the virus's metabolic hijacking of the host’s energy pathways. Mitochondrial efficiency is gradually compromised as the virus begins to reprogram cellular respiration processes to favor anaerobic and thermogenic energy cycles—adapted for viral replication rather than host survival. This shift results in an abnormal accumulation of lactic acid, leading to persistent muscle soreness, cramps, and disorientation even under mild exertion. Simultaneously, the virus triggers an endocrine imbalance. Affected individuals experience fluctuations in core body temperature, often accompanied by periodic fevers alternating with sudden chills. These temperature anomalies correlate with episodic surges in viral replication cycles, during which host cells are rapidly overwritten or consumed. Hormonal disruption may also cause appetite suppression, dehydration, and irregular circadian rhythms. The central nervous system begins to exhibit preliminary signs of viral influence shortly thereafter. Infected hosts frequently report migraines, short-term memory disruption, and sensory distortion—particularly in vision and auditory processing. In more advanced cases, early-stage hallucinations or dissociative episodes may occur, indicating the virus’s early attempts at interfacing with the host's neural circuitry.
Internally, diagnostic imaging and tissue sampling reveal unexplainable micro-lesions across major organs—especially the liver, lungs, and lymphatic system—coupled with abnormal growths resembling fibrotic scaffolding or foreign mycelial filaments. These structures are theorized to act as nutrient sinks or transmission conduits, facilitating both systemic infection and inter-host spore dispersal. Despite these emerging symptoms, many infected individuals retain cognitive coherence during this phase, often attributing their condition to more mundane causes such as exhaustion or flu. This delayed recognition contributes significantly to the virus’s spread, particularly in densely populated environments, and hinders containment efforts until external signs become visibly pronounced.

Visible Symptoms

Visible symptoms of K5-63 infection typically begin to manifest after the internal integration phase has advanced beyond the point of immunological resistance and systemic control. These symptoms mark the transition from covert infection to overt transformation and often coincide with the host’s loss of physiological autonomy.
The first outward signs include a pronounced discoloration of the skin and mucous membranes. A bluish-gray pallor begins at the extremities—fingers, toes, lips—and spreads centrally as peripheral circulation is compromised. This discoloration is accompanied by subdermal vascular swelling, creating a web-like network of darkened veins across the surface of the skin. The veins pulse erratically as viral activity intensifies within the circulatory system, particularly during aerosol spore production cycles. Shortly thereafter, abnormal keratinization begins. Patches of skin thicken, harden, and take on a reflective, chitinous sheen, particularly around the joints, clavicle, and cranial plates. These formations appear to be exogenous tissue growths—hybridized structures that blend host biology with viral material. Though initially superficial, these growths deepen and expand over time, forming asymmetrical, armor-like protrusions that serve no biological function to the host but are theorized to protect developing viral nodes or spore sacs embedded beneath the dermis.
Concurrently, ocular transformation occurs. The sclera loses pigmentation entirely, resulting in a milk-white, clouded appearance, while the irises may darken or emit a faint bioluminescent glow due to structural alteration of retinal proteins. Vision becomes distorted and hypersensitive to light, with some subjects reportedly losing depth perception or exhibiting hyperfocus toward movement—potentially a behavioral adaptation favoring viral spread through host reactivity. Motor control begins to degrade by the time visible dermal alterations are fully present. Hosts display erratic, twitch-like movements and a staggering gait, often marked by asymmetrical muscle contractions or joint dislocations that fail to produce pain responses. This stage is accompanied by spontaneous vocalizations—moaning, incoherent murmuring, or guttural outbursts—likely a side effect of neural rerouting and partial suppression of higher brain function.
In the later stages, the most severe visual indicator is structural deformation of the host’s skeletal and muscular systems. Appendages may elongate or twist, bones fracture and reform at unnatural angles, and extrusions of fused bone and hardened viral tissue erupt from the back, limbs, or jawline. These changes do not follow any recognizable biological architecture and are presumed to be driven by the virus’s internal directive—possibly linked to an unknown logic or coordination function rather than individual survival. Notably, despite the grotesque nature of these changes, many hosts remain alive well into the late stages, albeit in a state of limited consciousness or full neurological subjugation. Some retain fragmented memories or motor responses associated with their previous identity, though these are fleeting and non-functional. The transformation continues until the host either expires from structural failure or is entirely repurposed as a stationary spore vector or mobile bio-conduit, depending on environmental conditions and viral directive.

Alteration

Complete biological alteration marks the terminal phase of K5-63 infection, in which the host is no longer biologically or neurologically autonomous. At this point, the virus ceases to merely parasitize the host and instead fully repurposes its body as an adaptable, self-replicating vector platform. The process is neither random nor merely degenerative—it is systemic, purpose-driven, and unfolds according to an internal logic that remains poorly understood.
The onset of alteration is signaled by an acceleration in cellular remodeling. Viral elements embedded within the host genome begin expressing a suite of synthetic proteins and extracellular matrices that override native tissue functions. Muscular tissues are restructured, often torn down and rebuilt with hyper-dense fibrous material that grants increased tensile strength and resistance to trauma, though this often comes at the cost of fine motor control. Inorganic-seeming growths—comprised of complex silicate-laced organics—emerge along the spine, chest, and extremities, forming semi-rigid, asymmetric anatomical structures with no parallel in known biology. Bone density increases dramatically as the skeletal frame expands or contorts to support new viral superstructures. In many cases, new limbs or tendrils form, sprouting from the scapulae, ribs, or along the vertebral column. These appendages may terminate in hardened points or multi-jointed claws, possibly intended for traversal, manipulation, or defense—though no uniform morphology has been cataloged. Each host appears to undergo a unique pattern of alteration, possibly directed by localized environmental conditions, internal viral load, or other inputs unknown to current xenobiological modeling.
Internally, vital organs are either augmented or rendered obsolete. The respiratory and digestive systems often collapse or fuse into an undifferentiated organ-mass optimized for gas exchange, thermal regulation, or spore generation. The cardiovascular system is subsumed by a network of pulsating, bio-luminescent conduits through which viral fluid circulates independently of the original heart-lung loop. Some infected subjects exhibit no discernible heartbeat or oxygen requirements in later stages, suggesting a partial decoupling from aerobic metabolism. The brain undergoes profound neurostructural reconfiguration. Cortical layers are thinned and replaced with branching neural filaments that interface with embedded viral nodes distributed throughout the cranium and spinal cord. These filaments serve as both signal processors and memory conduits, enabling the host to function as a distributed computational node in service of the virus’s larger behavioral schema. Traditional brain functions such as self-awareness, language, or pain recognition are either suppressed or permanently erased. However, rudimentary motor coordination and environmental responsiveness remain intact, allowing altered hosts to operate independently if necessary.
Of particular note is the formation of crystalline growths within and around neural tissue. These formations emit faint electromagnetic pulses, measurable but poorly understood, and may serve as a communication medium among altered hosts. In several documented cases, clusters of infected individuals displayed coordinated movement patterns and parallel behavioral responses without any detectable external communication—suggesting the presence of an emergent group-level intelligence or synthetic hive function. Once the alteration reaches its terminal phase, the host body no longer exhibits cellular death in the traditional sense. Damaged tissue is either absorbed or rapidly replaced with reconstituted viral biomatter. While the process is not regenerative in the natural sense, it does confer a form of self-repair—albeit crude and limited to structural integrity rather than restoration of original function.
The end state is a hybrid construct: neither fully biological nor synthetic, no longer individual nor entirely autonomous. These altered hosts are referred to informally as “constructs” or “repurposed entities” by containment teams, though these are descriptive rather than taxonomic terms. They represent the final, irreversible stage of the K5-63 infection, at which point the subject's original identity and biology have been effectively erased, and all functional systems repurposed for goals not yet fully understood.

Hive Mind

As hosts progress into the later stages of K5-63 infection and undergo complete biological alteration, evidence increasingly suggests the emergence of a distributed cognitive framework—a non-localized hive mind that binds infected entities into a unified behavioral network. While initial infection appears individualized and largely autonomous, advanced-stage constructs begin exhibiting coordinated behaviors indicative of shared awareness, synchronized responses, and a form of collective purpose not evident during earlier phases. The hive mind does not manifest through audible speech or conventional transmission. Instead, subjects display what can only be described as pattern-linked cognition: simultaneous environmental responses, mirroring of physical actions, and route optimization in unfamiliar terrain without prior mapping. In some observed instances, constructs separated by considerable distance altered movement patterns or posture in tandem, despite the absence of direct visual, auditory, or electromagnetic signals. This implies a deeper connectivity—likely embedded within the altered neuroviral architecture—facilitating subquantum, chemical-neuromagnetic, or unknown quantum-interference-based communication.
Constructs within the hive appear to stratify functionally, though no rigid hierarchy has been observed. Some act as mobile scouts or infection vectors; others remain stationary, embedded in walls, machinery, or organic terrain—serving potentially as anchors or relay nodes within the collective network. These stationary entities, while biologically inert by conventional standards, pulse with low-frequency electromagnetic activity and continue generating viable spores long after host vitals have ceased. They may function as memory nodes or command processors within the larger system. The hive mind is not static—it adapts. Encountered resistance, containment protocols, or environmental threats are not merely observed but rapidly internalized. Future construct behavior then adjusts accordingly, often with disturbing precision. Infected entities will avoid known ambush zones, bypass decontamination traps, and in some cases, sabotage or manipulate control systems in ways that imply retained technical or tactical memory. This level of behavior strongly suggests a form of memory integration across the network, wherein information acquired by one construct becomes accessible to all others.
Moreover, hosts who perish during early or mid-stage infection but are later exposed to the virus can still be drawn into the hive’s operational structure. Bodies once thought neutralized have reactivated in the presence of active nodes—implying that K5-63 does not merely infect the living, but can manipulate and reconfigure necrotic tissue as part of its collective biomass. These reanimated forms are less mobile, but often act as environmental traps, lures, or proximity-triggered dispersal agents. It is currently unknown whether the hive possesses a centralized intelligence or is instead governed by a fully distributed logic. Constructs do not display signs of hierarchy, emotion, or recognizable leadership; their movements are silent, efficient, and uniformly purpose-driven. There is no evidence of individual will. Instead, they appear to act under a singular, emergent directive—expansion, replication, and assimilation. Whether this is the result of alien design, unintended evolution, or a naturally forming neural network is the subject of ongoing speculation.
More troubling is the possibility that the hive mind operates on a time-delayed intelligence curve—one that increases in sophistication as additional hosts are assimilated. With each new construct, the complexity of behavior, the speed of adaptation, and the coherence of actions appear to escalate. This suggests the hive mind is not fixed in capability but instead dynamically scalable, growing in power with each biological addition, each absorbed memory, and each environmental stimulus. Infected individuals within this network retain no agency. Attempts to sever individuals from the collective via amputation, sedatives, or neural inhibitors have all failed. Even partial constructs exhibit reflexive violence if isolated, and some seem to self-terminate or dissolve into virally active matter when cut off from the hive for prolonged periods—potentially to deny containment efforts any usable biological data.
Whatever intelligence lies behind the hive mind—whether artificial, adaptive, or emergent—it is wholly alien in behavior and intention. Communication attempts have produced no results; no construct has responded to language, symbols, or emotional stimuli. The virus does not seek to negotiate, bargain, or dominate in the conventional sense. It simply acts—calculating, precise, and methodical—in pursuit of an unknown directive that disregards the boundaries between life and death, self and other.

Hosts & Carriers

K5-63 demonstrates an extraordinary capacity for host compatibility across a vast range of biological organisms, displaying an almost indiscriminate ability to infect, alter, and repurpose complex lifeforms. The virus exhibits a strong affinity for environments containing moisture, bioavailable carbon, and thermal gradients consistent with endothermic organisms—conditions most commonly found in sapient and semi-sapient species. However, its tolerance for biochemical diversity extends far beyond baseline assumptions, suggesting that the virus was either originally engineered for broad-spectrum application or evolved through directed pressure toward cross-species adaptability.
The ideal hosts for K5-63 infection are mid-to-large bodied organisms with dense vascular systems, high neural mass, and moist tissue environments that facilitate intracellular diffusion. Endothermic beings are preferential due to their stable thermal envelopes, which accelerate viral replication and optimize spore production cycles. Once infected, these hosts undergo full transformation over a period of several weeks, ultimately serving as advanced biological constructs within the collective hive mind. However, not all organisms infected by K5-63 become full constructs. A significant number instead function as asymptomatic carriers—entities in which the virus integrates silently, remaining in a dormant or partially active state without triggering full alteration. These carriers are fully infectious and capable of releasing airborne spores through respiration, perspiration, or dermal micro-shedding. Some may never exhibit visible symptoms, yet still act as key vectors in long-distance transmission chains. The latency and silence of this carrier phase is arguably the most dangerous property of the virus, allowing entire populations to become compromised without detection until the critical saturation threshold is reached.
Hosts with compromised immune systems or unique neurochemical balances may experience incomplete alterations. These partial transformations often result in grotesque chimeric outcomes—beings locked in states of anatomical instability, unable to complete the viral directive yet too altered to retain biological identity. Such entities are often violent, unstable, and serve primarily as shock vectors, spreading the infection through erratic aggression and bodily rupture. Despite lacking the cohesion of full constructs, these aberrant forms often serve strategic roles within outbreak zones, forcing chaos and dispersal patterns favorable to viral spread. In rarer cases, non-animal lifeforms—including certain high-moisture plant analogs and simple microbial colonies—have shown partial susceptibility to viral colonization. While such hosts do not exhibit transformation, they can become secondary incubation zones, producing airborne spore clouds or acting as passive infection platforms for days to weeks. These passive vectors form a secondary ecological layer to the viral threat, allowing the infection to persist in sterilized zones or reemerge following containment collapse.
Of particular note is the virus’s ability to integrate memory and behavior through host assimilation. Advanced constructs often exhibit retained motor routines, reflexive actions, or environmental familiarity associated with their pre-infection identities. This residual behavior serves both camouflage and tactical advantage—constructs navigating complex terrain, accessing locked infrastructure, or mimicking benign biological cues to approach uninfected individuals. While these actions may appear intentional, they are not conscious; they are memory traces repurposed by the virus as utility code, reinforcing the notion that host cognition is not erased, but overwritten and redeployed in service of a higher directive. The virus does not display moral distinction between host types. Sapience, intelligence, or social bonds offer no protection. Family members, crewmates, or even entire command structures have been documented falling in synchronous sequence as the infection propagates invisibly through shared air, surfaces, and biometric interfaces. Emotional appeals, recognition attempts, or psychological triggers have universally failed to reach altered hosts—once neural integration passes the threshold, identity is lost, and function becomes singular: to spread, to adapt, and to transform.

Treatments

There is no known treatment, cure, vaccine, or antiviral agent effective against the K5-63 virus at any stage of infection. All efforts to disrupt the virus’s life cycle—biologically, chemically, or physically—have met with failure. Its structure is not only resistant to conventional immunological pathways but appears to actively adapt when exposed to foreign biological agents. Attempts at targeted neutralization through gene-editing, viral inhibitors, or nanomedicine have resulted in rapid counter-adaptation, tissue rejection, or systemic host collapse.
The virus's core complexity lies in its recombinant genetic payload—a semi-synthetic helix matrix that rewrites host DNA using encrypted, self-replicating code. This matrix is shielded by an advanced protein sheath that resists denaturation at both high and low thermal thresholds, rendering heat-based sterilization ineffective unless total incineration is achieved. Even when isolated in vitro, the virus persists in a dormant state for extended periods, reactivating once ideal host conditions reemerge. Pharmacological approaches have proven not only futile, but in some cases catastrophic. Broad-spectrum antivirals and immune enhancers have, in several instances, accelerated viral activity—suggesting that the virus interprets chemical threat as a trigger for faster host restructuring. Suppressive regimens such as immunosuppressants, cytotoxins, or radiation therapies only delay visible transformation while increasing internal tissue instability, often resulting in catastrophic failure and spontaneous aerosolization.
Physical intervention offers no advantage. Surgical removal of infected tissue does not prevent further spread, as the virus replicates systemically and is not confined to any single organ or region. Amputation, organ excision, and induced coma protocols have all resulted in resumed viral activity once the subject stabilizes. In rare instances, infected subjects have displayed cellular regrowth in the absence of functional support systems—an outcome attributed not to recovery, but to viral control of regenerative mimicry. These subjects were no longer human in any recoverable sense. Neurological intervention has likewise failed. Attempts to sever infected individuals from the viral collective—via electromagnetic pulses, chemical inhibitors, or cortical suppression—have only resulted in violent neurological backlash or host expiration. In later stages, the virus fully assimilates neural architecture, rendering any distinction between host and virus meaningless. Once this threshold is crossed, the subject ceases to be treatable. It is no longer infected—it is transformed.
The only consistently successful method of containing the K5-63 virus is the total and irreversible destruction of the host organism. This includes complete biological incineration, disintegration, or disassembly at a molecular level. Anything less risks residual viral activity, reactivation, or unintended propagation through environmental contact. Even isolated remains can emit spores under specific conditions, and secondary reanimation of partially-altered corpses has been recorded under favorable microbial and thermal stimuli. Due to the virus’s ability to remain dormant and undetected during its latency phase, no viable early-intervention window exists. Standard quarantine procedures are unreliable, as asymptomatic carriers can pass all diagnostic scans while actively shedding virions. Any delay in response—whether due to uncertainty, containment protocol, or ethical hesitation—almost invariably results in widespread contamination.
The grim reality is this: K5-63 is not a disease to be cured—it is a mechanism of transformation. It does not merely consume life; it rewrites it, adapting each host into a biological extension of its expanding network. What it infects, it converts. What it converts, it retains. Once integration begins, the process cannot be reversed, reasoned with, or arrested. Medical science, in its current state, is simply not equipped to counter a viral entity that does not abide by the rules of terrestrial biology.
As such, no treatment options are recognized. The protocol is isolation, sterilization, and absolute containment. Anything less is failure.

K5-63 Virus

Origin

Engineered

Cycle

Chronic, Acquired

Rarity

Unique

First Outbreak

19th September 2726 (contained)

Second Outbreak

3rd May, 2745