Canine Hematophagic Virus

The Canine Hematophagic Virus (CHV) is a single-stranded RNA virus belonging to the family mononegavirales. It is a zoonotic virus capable of infecting canines and potentially humans. CHV is notable for its ability to integrate its genome into the host's DNA, causing profound physiological transformations that result in blood-feeding Chupacabras.
CHV is highly efficient at infecting host cells, capable of infecting nearly every living cell in the body except for red blood cells. The virus enters host cells via endocytosis and utilizes the angiotensin-converting enzyme 2 (ACE2) receptor for cellular entry. Once inside, it manipulates the host's genome, leading to extensive physiological and anatomical changes.
The virus appears to have originated in humans before mutating to infect canines, potentially carrying over adaptations from its human host. This has resulted in infected canines developing some human-like traits, such as limited bipedalism and increased forelimb dexterity.
CHV infection progresses through three distinct stages, each marked by increasingly dramatic physical and behavioral changes in the host. These changes ultimately result in a creature highly adapted for blood feeding, with significant alterations to its digestive, skeletal, and muscular systems.

Transmission & Vectors

• Likely transmitted through bite or contact with infected bodily fluids
• Zoonotic, capable of infecting both canines and potentially humans

Causes

• Infection by the Canine Hematophagic Virus (CHV)

Symptoms

Stage One (Days 0-21):

• Mild or absent symptoms initially
• Fever, lethargy, and loss of appetite by day 3
• Decreased heart rate and potential comatose state (18-36 hours)
• Loss of fur and hyperkeratosis of the skin
• Ravenous hunger and extreme aggression
• Dorsal bone growths (osteophytes)
• Elongation of eyeteeth
• Bulging eyes with loss of iris pigmentation

Stage Two (Weeks 3-6):

• Restructuring of digestive system for blood processing
• Shortening of intestinal tract
• Enhanced kidney function
• Changes in oral palate and jaw structure
• Development of powerful suction mechanism for feeding
• Continued growth of dorsal osteophytes
• Complete loss of fur
• Increased fast-twitch muscle fibers

Stage Three (Several weeks after Stage Two):

• Shift towards limited bipedalism
• Lengthening and reorientation of hind limbs
• Broadening of pelvic girdle
• Increased articulation in forelimbs
• Neurological adaptations for new body plan

Treatment

None known currently.

Prognosis

• High mortality rate in the first stage of infection
• Survivors undergo irreversible physiological transformations
• Long-term survival prospects not specified

Sequela

• Permanent physical transformation into a blood-feeding canine
• Loss of normal feeding behaviors
• Increased aggression and potential loss of cognitive functions
• Nocturnal behavior
• Inability to return to normal canine lifestyle

Epidemiology

• Initially observed in Puerto Rico (Moca)
• Later spread to Colorado and surrounding states
• Potential for wider spread noted but extent unknown

History

• Believed to have originated in humans and mutated to infect canines
• May have gone undetected in humans for thousands of years
• First major outbreak documented in Moca, Puerto Rico in 1975

Cultural Reception

• Primary hosts: Canines (including domestic dogs, wolves, and coyotes)
• Potential to infect humans, though extent and effects not fully explored

Secret (available to Patrons at 'Stack of Potatoes' and higher):

Origin

Mutated

Rarity

Extremely Rare