The Chupacabra

On the night of February 25, 1975, the eerie silence that hung over the town of Moca, Puerto Rico, was broken by a chilling shriek—a sound so terrifying it seemed nearly otherworldly. The next morning, a grim discovery awaited the townsfolk: fifteen cows, three goats, two geese, and a pig, all lifeless, their bodies punctured and drained of every last drop of blood. The newspapers dubbed the unknown predator el Vampiro de Moca—the "Moca Vampire." And this so-called “vampire” wasn’t done yet. Over the next two months, the cold light of daybreak would reveal many more animals, each found entirely exsanguinated.
Theories as to this predator’s true origin and identity varied greatly—some said a canine, some said a snake, while others claimed that it was an extraterrestrial.
It my intention to lay these speculations to rest. My investigation has revealed the truth of these attacks, and while it is not as… sensationalized as an alien invasion, the reality is no less astounding, and the full implications of this creature’s existence are, I must admit, still outside even my own understanding.
Bear with me for this time, my valued listener, as I present my full findings on the deaths in Moca . . . as I fear they will not be the last.

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I will waste no time in presenting my conclusion–the Moca Vampire, as it were, is not an otherworldly being, nor is it an organism unexplainable by rational scientific methods.
But to truly understand what it is, we must understand the mode and method of its attacks.
The investigation of precisely this question was thrust upon me just a few days after the initial attacks were reported.
I must admit that though I arrived in Puerto Rico within the week, the timing of my journey was already… undesirable. Under normal circumstances, my team and I would have begun an investigation of this kind within hours, as, should the reports turn out to be true, a rapid response is key to successful media suppression.
My superiors did what they could, but by the time I had established preliminary findings, word had already spread, and as of now, I suspect that a legend has already been born.
In any case, I was able to examine the corpses of 28 animal victims, and to confirm that each mammalian body had been entirely drained of blood. In almost every case, the only evidences of an outlet were a pair of small holes at the neck, though often surrounded by surface-level lacerations.

  As the specimens I examined grew in number, I began to feel increasingly uneasy. It may come as a surprise to know that these were not the first corpses I had observed with a chillingly similar cause of death, but they were the first . . . non-humans. At the time, I wasn’t sure if the two circumstances could possibly be related, but though that mystery is still unfolding, the similarities between these and Dr. Foster’s death are and were alarming. Given the size of some of these creatures, such as a pig and cow, and the lack of compression fractures in the rib cages of the others, I ruled out the bat and snake theories that had been presented to me, though I was happy to let the media run with these.
I launched an extensive observation initiative, and within mere days, I had found my first specimen. In some ways, I wish it had ended there.
In actuality, the so-called Moca Vampire is a canid, though the exact species varies. One could claim that the real predator is the virus that infects them—one that causes such a disturbing transformation in its host that they could very nearly be considered an entirely new organism. This is especially true of the almost unrecognizable late stages. But I’m getting ahead of myself.
In truth, deciphering the phylogeny and function Canine Hematophagic Virus, or CHV, as I have named it, has proven exceptionally difficult. Had Marcus remained with the department, the process may have gone more smoothly, but even so, I have obtained enough verifiable information to present here.

The Virus

  CHV is a single-stranded RNA virus, what appears to be a zoonotic member of the family mononegavirales, sharing distinct similarities with another member of that family—but we will return to that in a moment. CHV is a master of genetic manipulation, capable of integrating its own genome into the host's DNA, triggering profound physiological transformations that result in the eerie, blood-siphoning canines somewhat aptly called “vampires.”
Amazingly, and in contrast to most viruses, which are highly targeted to specific host cell types, CHV appears to be able to infect every living cell in its host, with the notable exception of red blood cells.
Though my research into the mechanisms of this virus’s infection will likely continue for some time, it appears that the virus enters the host cell via endocytosis, wherein the virus essentially “hijacks” the host cell, rather than triggering lysis. In detail, the virus utilizes the angiotensin-converting enzyme 2 receptor for cellular entry. The ACE2 receptor's conserved structure across mammals allows the virus, which I hypothesize specialized in humans first, to bind and gain entry into the canine cells.
Once inside the cell’s cytoplasm, CHV begins its replication cycle. There, the virus's RNA-dependent RNA polymerase transcribes the negative-sense RNA genome into positive-sense RNA. This serves as a template for the synthesis of viral proteins and the replication of new viral genomes. Put simply, thanks to RdRp’s lack of proofreading, a novel protein with integrase-like activity appears to have arisen from a mutation in one of the viral genes.
The CHV, appearing to behave remarkably like a retrovirus, reverse transcribes its RNA genome into cDNA, which integrates into the host's genome. During this process, a host gene adjacent to the integration site is incorporated into the viral genome. This gene, when expressed in canines, leads to numerous physiological changes. The virus then transcribes this combined genome back into RNA, packages it into new viral particles, and releases these particles to infect other cells. The incorporated host gene, now part of the viral genome, is inserted into the genome of newly infected cells. If activated, it could lead to the expression of new physiological traits in the host. And indeed, it appears to do just that.
In short, the Canine Hematophagic Virus is an insidious and ultra-efficient agent of infection, spreading to nearly every system and tissue within the canine body within mere hours.
The resulting physiological changes are nothing short of staggering, and if these changes are even a glimpse of what might occur in other species—namely, humans—then, my valued listener, I hope that my sense of anxiety will soon appear warranted.

The Transformation

 
Beginning on day zero, viral proliferation and infection takes place over roughly two to three days. During this time, symptoms are mild or may be absent altogether. As the virus infects the pituitary gland, thyroid, and other adjacent hormone-regulating structures, metabolism increases, greatly accelerating systemic infection. By day three, symptoms frequently include fever, lethargy, and loss of appetite. Heart rate dramatically decreases during this time, and may even lead to a prolonged, nearly comatose state, lasting between 18-36 hours.
The immune response triggered by the infection leads to systemic inflammation universally resulting in the loss of fur, as well as hyperkeratosis of the skin. This scaly appearance is likely driven by the upregulation of keratinocyte growth factor in response to the infection itself, which in turn, leads to the overproduction of keratinocytes and the formation of a relatively thick, hardened dermal layer. It is this side effect that has led many to dismiss sightings of early-stagers as simply being infected with mange.
On days four through seven, victims of the infection begin to become more alert, and often exhibit a ravenous hunger. Likely due to the infection of brain cells, signs of neurological symptoms also appear, such as confusion and extreme aggression—a very dangerous combination.
By the end of the first week, almost universally, the virus has begun to alter the genetic makeup of its hosts’ cells, and the first disturbing signs of physical transformation become apparent. In the second week, the sequence of anatomical changes is less predictable, but within 21 days, the changes I consider to be the hallmarks of “stage one” are complete.
Within that time, skin along the dorsal region begins to erupt with growths of bone tissue. These highly abnormal osteophytes appear to be triggered by the virus’s manipulation of the host’s bone morphogenetic protein signaling pathway, though as of yet, these growths serve a purpose unknown to me. It’s possible that they serve a defensive function, though more time spent studying these creatures in the wild would be necessary to say for sure.

 

  It is in this stage that we see the first of the extensive craniofacial changes that become more apparent as the transformation progresses. The eyeteeth begin to elongate, undergoing uncharacteristically rapid growth, facilitated by specialized cells known as ameloblasts. These cells journey through the narrow channels within the dentin and crown of the tooth, depositing additional enamel at the tip to form a sharp, elongated ”fang.” Of course, this altered dentition is crucial for these canines’ post-infection feeding habits, a point to which we’ll return shortly.
Lastly, the infection often leads to an overproduction of collagen in the sclera of the eyes, likely driven by the upregulation of TGF-beta, which causes the eyes to bulge and appear larger. Additionally, the virus appears to downregulate the expression of melanogenic enzymes such as tyrosinase in the iris, leading to a loss of pigmentation, and enhancing the victims’ increasingly haunting visage.
I should note that mortality rate in the first stage is high, and likelihood of survival is difficult to predict. For those that do survive, however, even more drastic changes await.

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While the changes initiated in the first stage are drastic, it is the second stage that truly unleashes the horror encountered by so many Puerto Ricans earlier this year. First and foremost is a nearly complete restructuring of the digestive system, fully adapted to the large-scale processing of blood.
At this stage, full dissection was crucial to my study, though I must admit my regret of the loss of more than one of these fascinating creatures. But alas, as I have come to find, freedom of choice is a true luxury.
The CHV appears to induce a significant shortening of the intestinal tract, a modification that enhances the absorption and processing of nutrients from a liquid diet, much like the adaptations observed in other hematophagous organisms, such as vampire bats.
Simultaneously, the kidneys become remarkably proficient at filtering and excreting the surplus nitrogen resultant from a high-protein diet. This is a critical adaptation, as the elevated protein content in blood could otherwise lead to a hazardous accumulation of nitrogenous waste products–primarily urea.
The virus also appears to trigger alterations in the host's genome and gut microbiome to counter the low nutrient availability inherent in a blood-based diet. Concurrently, the gut microbiome undergoes a shift, with genes associated with energy and carbohydrate metabolism becoming more prevalent. Astoundingly, this indicates a symbiotic relationship between the host's genome and gut microbiome, working in concert to maximize energy extraction from the blood.
Finally, the host's immune system also undergoes significant changes. The virus appears to upregulate genes involved in immune response, potentially as a countermeasure to the increased risk of exposure to blood-borne pathogens. The gut microbiome reciprocates this adaptation, with potentially protective bacteria becoming more prevalent.
But of course, as carnivorous creatures, canine anatomy already lends itself to feeding on other animals. However, in the case of those infected by CHV, these digestive system alterations are, perhaps, a direct result of the changes that occur in the mouth.

 

  Up to a point, roughly 7-14 days after infection, the canine host exhibits no major changes to its dietary or hunting habits. Over the period of approximately two weeks, however, the oral palate undergoes significant morphological changes. The palatine bones, which form the anterior part of the hard palate, become more flexible. This is likely due to the virus-induced upregulation of genes involved in bone remodeling, such as those encoding for osteoclasts and osteoblasts, cells responsible for the breakdown and formation of bone tissue, respectively. This, in turn, facilitates the formation of a more pronounced *buccal* cavity. This expanded cavity, combined with enhanced muscular control in the mouth and throat, allows the infected canine to generate a powerful suction force, something like the buccal pump mechanism seen in certain species of fish and amphibians.
Simultaneously, the maxillary bones, which house the upper dentition and form the lateral boundaries of the hard palate, also undergo changes. Here, the virus appears to induce an increase in the density and strength of these bones, providing a more robust framework for the enlarged canines and the increased mechanical stress associated with the buccal pump feeding mechanism.
In practice, the process of feeding is always undertaken nocturnally—a behavior suited to existing canine circadian rhythms—and can be described in a series of steps:
First, because the hematophagous canine’s saliva contains both a glycoprotein anticoagulant, called draculin, and proteins that block sodium channels in the nerves of the skin, numbing the area of the bite, its victims are often entirely unaware of their own exsanguination. Indeed, the telltale twin pricks in the neck are often nearly surgically precise, rarely waking the victim at all.
Of course, for those canines in the earliest stages of transformation, the bloodletting is not nearly so delicate, and may be accompanied by additional lacerations, signs of struggle, and may even appear to be a traditional predator attack.
Once the oral cavity has undergone sufficient restructuring, however, the feeding pattern becomes much more refined.

  After making the incision over a major artery in its victim, the hematophagous canine will open its mouth, expanding its buccal cavity by lowering the floor of the mouth, which is primarily composed of the tongue and some muscle, creating a low-pressure area inside the mouth. This, in turn, causes blood to be drawn up from the wound and into the mouth.
The canine then compresses the buccal cavity by raising the floor of the mouth, now creating a high-pressure area.
Finally, this higher pressure forces the blood down the throat and into the stomach.
In short, the process is similar to that of inhalation in exhalation in the lungs, and, as many livestock owners came to see for themselves, it is a brutally efficient means of blood extraction.
However, I should note that the while volume of circulating blood in the mammal victim can vary greatly based on its size, it is often over five liters, and the average canine stomach can only hold one to two liters of liquid at any one time.
As a result, infected canines must feed over long periods of time, usually several hours. However, of course, multiple infected individuals can make quick work of many animals, as is evidenced by the numerous reports.
Of course, taken on their own, these anatomical changes might have led to respiratory problems. But once again, the virus provides a solution. The shape and composition of cartilage in the temporomandibular joint is altered to allow for greater flexibility, and new layers of bone are laid down in the mandible in order to cope with the strain exerted by the enlarged muscles within.
Elsewhere, the dorsal osteophytes continue to elongate, and if any fur remains on the body, it has likely been entirely shed.
Interestingly, close examination of infected muscle tissue has revealed what appears to be a proliferation of fast-twitch muscle fibers–so much so that they made up close to 90% of the total fibers in the tissue I collected. Undoubtedly, this makes these infected canines capable of extraordinary bursts of speed, though, I suspect, they are more susceptible to fatigue.
And so, with these extreme biological alterations complete, the canine has come to the end of the second stage of infection.
For a time, I thought this to be the final stage, as those individuals in my direct observations underwent no additional perceptible changes for several weeks. In fact, I was content to consider this particular investigation complete, and after a short time, had returned to the mainland.
Then, just a few months later, my department was forwarded a communication from a concerned senator, originally directed to the FBI, that outlined a string of cattle deaths in Colorado and several surrounding states—wherein each carcass had been entirely drained of blood.
Needless to say, I set out once again, unsure of what I would find. And, once more, I constructed several places of observation.
Frankly, though I already suspected a spread of the virus as the culprit, I wasn’t entirely prepared for what I found.
The circumstances of my findings are best left for another time. But in short, what I found there was an undeniable third stage of infection, directly observed in canis latrans, or the coyote.
Like the specimens in Puerto Rico, these infected exhibited dorsal osteophytes, altered dentition, severe hair loss, and pronounced bulging of the eyes.
However, in these specimens, likely over a period of many weeks, the virus appears to have also fundamentally altered the entire canine body plan.

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  Indeed, through an extensive reorganization of the musculoskeletal system, I have observed a shift towards a form of limited bipedalism, likely mediated by the virus's influence on host gene expression. The skeletal changes are most pronounced in the hind limbs, which lengthen and reorient to support an upright posture. The femur, tibia, and fibula hypertrophy in direct response to the increased load-bearing demands of bipedalism, while the pelvic girdle, specifically the ilium, broadens and the acetabulum repositions.
Accompanying these skeletal alterations are significant muscular*adaptations. The gluteus maximus, medius, and minimus, which play a key role in maintaining an upright posture, increase in size and strength, while the biceps femoris, semitendinosus, and semimembranosus, together crucial for hip extension and knee flexion, also hypertrophy to support the altered gait mechanics of bipedal locomotion.
Behaviorally, I have observed the quadrupedal locomotion is still preferred by infected individuals, especially when attempting long-range travel. However, the enhanced ability to stand and even “hop” is likely extremely useful in both locating prey, sentinel behavior, and enhanced traversal of difficult terrain.
Amazingly, the forelimbs, while retaining their basic canine structure, exhibit somewhat increased articulation, particularly in the carpal and metacarpal regions. This shift towards a slightly more manipulative role is facilitated by elongation of the phalanges and increased flexibility in the joints. The flexor and extensor muscles of the forelimbs, responsible for the bending and straightening of the paw, respectively, adapt to allow for more precise movements.
Together, these changes provide a significant advantage for a hematophagic predator, allowing for more precise control when targeting and accessing blood vessels in their prey.

 

  But of course, these physical changes must also be accompanied by significant neurological adaptations–and so they are. The areas of the motor cortex associated with the limbs expand, facilitating more precise control of the newly dexterous forelimbs and the altered gait mechanics, and the sensory cortex adapts to process increased tactile information. Deep brain structures involved in movement initiation and control, such as the basal ganglia, are also affected.

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By now, the question that burned in my mind is likely burning in yours as well: *why* would the virus induce such drastic changes, especially when the canine body-plan is already designed for predation? Fortunately, while some of the advantages have already been described, I believe I have found the source of this genetic information.
It is my belief that this particular strain originated in humans, where it has gone undetected by mainstream science for perhaps thousands of years–though I suspect there is much more to discover. I dare not divulge too much information here, as my own research into the subject has so far been limited and, at times, actively discouraged.
Suffice it to say that the virus I have discovered in humans produces similar bloodlust. At some point, I hypothesize that the virus mutated in a way that allowed it to survive and eventually flourish in a canine host, perhaps passed along by a desperate attempt at obtaining sustenance.
In short, when the virus made the jump to canines, it must have carried over some of the adaptations associated with its former hosts’ lifestyle, including the shift towards bipedalism and increased forelimb dexterity.
This occurred through a mechanism known as horizontal gene transfer, wherein genetic material is transferred from one organism to another, non-offspring organism.
The genes involved in this process are numerous and varied, given the complexity of the adaptations observed, and will require much more study to understand fully.
In all honesty, the discovery of this virus, its likely origins, and its effects on this canine population are wonders of biology. Each successive insight seems to shatter established scientific notions, and while the process is exhilarating, at times, it is also… frightening.
I do not know what my future investigations will reveal, but for now, despite our best attempts to quell the spread of this particular strain and its infected victims, I can safely say that neither I, nor the public, has seen the last of the vampire of Moca.

Basic Information

Anatomy

Post-transformation:

• Enlarged jaw muscles.
• Altered cartilage in the temporomandibular joint for greater flexibility.
• New layers of bone in the mandible to handle strain from the muscles.
• Elongated dorsal osteophytes.
• Complete or near-total loss of fur.
• Predominantly fast-twitch muscle fibers in muscle tissue.
• Shift towards a limited bipedalism.
• Hind limbs are lengthened and reoriented to support an upright posture.
• Changes in femur, tibia, and fibula to support increased load-bearing.
• Broadened pelvic girdle and repositioned acetabulum.
• Enhanced forelimb articulation, especially in the carpal and metacarpal regions.
• Elongated phalanges and increased joint flexibility in forelimbs.

Genetics and Reproduction

• Evidence of horizontal gene transfer from humans to canines, introducing adaptations from former hosts.
• Numerous genes involved in observed adaptations, yet to be fully studied.

Growth Rate & Stages

• At least three distinct stages of infection.
• Second stage marked by pronounced anatomical changes, such as enlarged jaw muscles and dorsal osteophytes.
• Third stage involves bipedal adaptations and increased forelimb dexterity.

Ecology and Habitats

• Initially observed in Puerto Rico.
• Later found in canis latrans (coyote) in Colorado and surrounding states.

Dietary Needs and Habits

• Extreme bloodlust observed in infected canines.
• Some cattle carcasses entirely drained of blood, suggesting hematophagic tendencies.

Behaviour

• Capable of extraordinary bursts of speed, but potentially more susceptible to fatigue.
• While quadrupedal locomotion is preferred, infected canines can stand and hop.
• Enhanced traversal of difficult terrain.
• Use of bipedalism likely in sentinel behavior, locating prey, and accessing blood vessels in prey.

Additional Information

Perception and Sensory Capabilities

• Pronounced bulging of the eyes.
• Expanded sensory cortex to process more tactile information.

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