So, vampires would get bloodborne diseases, no?

By: Jacob Van Oorschot, Contributing Writer

Lately, I’ve been concerned for the health of vampires.  While I may not bear the curse of eternal life, I clearly have a bit of extra time on my hands. But seriously, vampires’ strictly-blood diet has me worried, due to all the blood-borne diseases they would be exposed to.

Bloodborne illnesses like HIV, Hepatitis B, and Hepatitis C are predominantly spread through unsterile needles, sexual contact, and from mother to child during pregnancy, birth, or breastfeeding (1). But surfaces of the body not covered in skin– like the genital tract, eyes, and (of particular interest for a feeding vampire) the inside of the mouth– can also be susceptible to infection by these diseases when exposed to infectious fluids. These surfaces are called mucous membranes, or, in fancy terms, “the mucosae”. In light of this, should your neighbourhood vampire be concerned with sanguine sicknesses? And if so, what precautions can they take?

The first pathogen that comes to mind is Human Immunodeficiency Virus (HIV), the infectious agent that causes AIDS. The virus is found in most bodily fluids of those infected, with the highest concentrations being found in the blood (2–4)! Even though we still don’t have a vaccine or  cure for HIV, proper antiviral treatment reduces the presence of the virus in the body to undetectable levels which largely prevents its transmission to others (5). This is good news for patients– and for any vampire who happens to feed on them. Even better, regimes of antiviral drugs called pre-exposure prophylaxis (PrEP) can be taken preventatively by healthy people at risk of exposure to the virus. PrEP is highly effective in preventing new infections (6)… in humans, at least. 

But would prophylaxis even be necessary for a vampire? To HIV, the oral mucosa presents a pretty hostile barrier to entry. It was long thought that HIV didn’t spread by infection through these tissues (7). However, it is now understood that while transmission is rare, it nonetheless occurs, especially when there are lesions, small cuts, or inflammation in the mouth (8). All that to say, the cautious vampire would be best advised to take advantage of PrEP.

Hepatitis B is another bloodborne infection that needn’t present an overwhelming risk for the conscientious vampire. Hepatitis B is a virus that can cause incurable lifelong chronic infection leading to liver damage and cancer, though acute infection is the more common outcome in adults with healthy immune systems (9). The virus is most concentrated in the blood of those infected (10) and the oral mucosa presents a susceptible site for infection (11). Uh oh! But there is good news. Unlike HIV, an effective vaccine exists for Hepatitis B (12) and a vaccinated vampire would have nothing to worry about with regard to Hepatitis B.

We can’t discuss bloodborne illness without talking about the Hepatitis C virus. Hepatitis C typically presents as a chronic illness (13), but unlike both HIV and Hepatitis B, it is readily curable. This is thanks to huge advances in treatment that have been made since the discovery of the virus in the 1980s, bringing cure rates near 100% (14)! However, for all our successes in treating it, we still lack an effective vaccine or other prophylactic treatment for the disease. While treatment for Hepatitis C is expensive– as in, tens of thousands of dollars expensive (15)– vampires always seem to be wealthy anyways (have you seen the Cullens’ home?). So this might be a test-often-and-treat-as-needed situation. Or, in a universe where vampires can store any blood they harvest before consuming it, the blood itself could be screened for the virus. The vampire would just need an insider at a lab somewhere. Though at that point, why not just siphon out of the existing supply at the blood bank? I digress.

Humans and vampires are biologically different, which might provide the latter some degree of protection from these diseases. Viruses are highly specialized infectious agents, and the bloodborne diseases discussed here tend towards particularly narrow host ranges (16–18). In other words, these viruses are the picky eaters of the infectious disease world. Although viruses take advantage of all sorts of tricks to evade their hosts’ immune systems, different species of animals have different immune systems, and a virus can only “know” a small number of tricks. Unfortunately for this investigation, vampire media rarely gets down to the specifics of immune system function, so any speculation here is purely conjecture. But there is one relevant and well-documented difference between vampires and humans: vampires are cold. And not just emotionally. In many a universe, vampires’ body temperature simply reflects the ambient environment; if the room they’re in is 20°C, their internal temperature will be around 20°C.

There is a dearth of real-world research into how vampires’ body temperature (or really, lack thereof) affects the ability of viruses to infect them. But we can draw some inferences from the existing literature. Researchers can block the entry of HIV into cells by incubating them at room temperature (19, 20). In contrast, to block Hepatitis C entry into cells, researchers refrigerate at 4°C (21). Cooler temperatures have been found to slow, but not completely stop replication of some viral relatives of Hepatitis C (West Nile, Dengue, and Zika viruses specifically), too (22). Whether this would be enough of an advantage for the vampires’ immune system to then clear the virus is a matter of speculation. 

But if we consider fungal infections, vampires’ lower body temperature could ultimately be the cause of their own demise. In contrast to viruses, which never allow themselves to look beyond the day-to-day grind of infecting the same host species over and over again, fungi have a lot more going on in their lives. Most make their living in the external environment. Any foray into human, animal, or vampire infection is more of a side hustle for them. As such, the vast majority of fungal species are adapted to the temperatures of the external environment, and are most comfortable growing between 12°C and 30°C (23). This partly explains why many common fungal infections we experience– think athlete’s foot, ringworm, and toenail fungus (24, 25)– are, while rather annoying, quite well behaved on the whole. They tend to stay superficial rather than penetrating deeper into the body where they could cause more serious harm. This isn’t by choice. Rather, our internal body temperature of 37°C is prohibitively warm for them (25, 26), so they must stick to our colder (27) superficial extremities. Think Journey to the Center of the Earth. Specifically, please, the 2008 movie with Brendan Fraser and Josh Hutcherson. 

But back to the original point, warm-bloodedness provides a barrier to infection against fungal pathogens (23, 28). To see what happens otherwise, we can look to frogs. The situation is grim. Since the 1970s, species after species of frog (as well as other amphibians) have been severely harmed or driven to extinction by the spread of chytrid fungi of the genus Batrachochytrium (29). Its maximum temperature for growth? 25°C (30) .

To sink our teeth back into the vampire discourse, let’s look at fungal infection in bats. White-nosed syndrome is a disease in bats caused by a fungus that only grows below 20°C (31, 32). Originating in Europe, it has been spreading and decimating bat populations in North America since its probable introduction in the first decade of this millennium (31). Echoing the most common fungal infections we see in humans, it tends to favour bats’ extremities, both (eponymously) their noses, as well as their ears. But bats, being mammals, are warm-blooded, and in fact tend to have body temperatures warmer than other mammals, as high as 41°C (33)! How come their body temperature doesn’t protect them from infection? Bats are big-time hibernators. Hibernation is all about conserving energy, so it comes with a precipitous drop in body temperature– often to ambient temperatures, which end up being between 1-16°C (31). 

The foundational decomposers of our world are fungi, which take (for the most part) dead organisms and render them unto to Earth whence they came. In a world presented with an undead threat such as vampires, it might ultimately be humble fungi, rather than flashy bloodborne viruses, that pull them back into the ground. Nature abhors the undead.

References

1. Blood Borne Infections. Public Health Ontario. https://www.publichealthontario.ca/en/Diseases-and-Conditions/Infectious-Diseases/Blood-Borne-Infections. Retrieved 3 January 2025.

2. Pilcher CD, Shugars DC, Fiscus SA, Miller WC, Menezes P, Giner J, Dean B, Robertson K, Hart CE, Lennox JL, Eron JJ, Hicks CB. 2001. HIV in body fluids during primary HIV infection: implications for pathogenesis, treatment and public health: AIDS 837–845.

3. Kordy K, Tobin NH, Aldrovandi GM. 2019. HIV and SIV in Body Fluids: From Breast Milk to the Genitourinary Tract. Curr Immunol Rev 15:139–152.

4. Pilcher CD, Joaki G, Hoffman IF, Martinson FEA, Mapanje C, Stewart PW, Powers KA, Galvin S, Chilongozi D, Gama S, Price MA, Fiscus SA, Cohen MS. 2007. Amplified transmission of HIV-1: comparison of HIV-1 concentrations in semen and blood during acute and chronic infection. AIDS 21:1723–1730.

5. Gardenier D, Kwong J, Colbert J. 2019. Does Undetectable = Untransmissable? The Journal for Nurse Practitioners 15:398–399.

6. Pre-Exposure Prophylaxis (PrEP) | NIH. https://hivinfo.nih.gov/understanding-hiv/fact-sheets/pre-exposure-prophylaxis-prep. Retrieved 1 January 2025.

7. Campo J, Perea M, Del Romero J, Cano J, Hernando V, Bascones A. 2006. Oral transmission of HIV, reality or fiction? An update. Oral Diseases 12:219–228.

8. Wood LF, Chahroudi A, Chen H-L, Jaspan HB, Sodora DL. 2013. The oral mucosa immune environment and oral transmission of HIV/SIV. Immunological Reviews 254:34–53.

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12. CDC. 2024. Hepatitis B Basics. Hepatitis B. https://www.cdc.gov/hepatitis-b/about/index.html. Retrieved 1 January 2025.

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17. Netter H-J, Chang S-F, Bruns M. 2008. Host-Range and Pathogenicity of Hepatitis B Viruses. Future Virology 3:83–94.

18. Lanford RE, Bigger C, Bassett S, Klimpel G. 2001. The Chimpanzee Model of Hepatitis C Virus Infections. ILAR Journal 42:117–126.

19. Gallo SA, Finnegan CM, Viard M, Raviv Y, Dimitrov A, Rawat SS, Puri A, Durell S, Blumenthal R. 2003. The HIV Env-mediated fusion reaction. Biochimica et Biophysica Acta (BBA) – Biomembranes 1614:36–50.

20. Henderson HI, Hope TJ. 2006. The temperature arrested intermediate of virus-cell fusion is a functional step in HIV infection. Virol J 3:36.

21. Tscherne DM, Jones CT, Evans MJ, Lindenbach BD, McKeating JA, Rice CM. 2006. Time- and Temperature-Dependent Activation of Hepatitis C Virus for Low-pH-Triggered Entry. Journal of Virology 80:1734.

22. Bisht K, te Velthuis AJW. 2022. Decoding the Role of Temperature in RNA Virus Infections. mBio 13:e02021-22.

23. Robert VA, Casadevall A. 2009. Vertebrate Endothermy Restricts Most Fungi as Potential Pathogens. The Journal of Infectious Diseases 200:1623–1626.

24. Taha M, Zaghloul AB. 2018. Superficial Fungal Infections, p. 37–51. In Orfanos, CE, Zouboulis, CC, Assaf, C (eds.), Pigmented Ethnic Skin and Imported Dermatoses: A Text-Atlas. Springer International Publishing, Cham.

25. Song Y, Li R. 2024. Chapter 146 – Superficial fungal infections, p. 2895–2904. In Tang, Y-W, Hindiyeh, MY, Liu, D, Sails, A, Spearman, P, Zhang, J-R (eds.), Molecular Medical Microbiology (Third Edition). Academic Press.

26. Barros ME da S, Santos D de A, Hamdan JS. 2007. Evaluation of susceptibility of Trichophyton mentagrophytes and Trichophyton rubrum clinical isolates to antifungal drugs using a modified CLSI microdilution method (M38-A). Journal of Medical Microbiology 56:514–518.

27. BIERMAN W. 1936. THE TEMPERATURE OF THE SKIN SURFACE. Journal of the American Medical Association 106:1158–1162.

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29. Berger L, Roberts AA, Voyles J, Longcore JE, Murray KA, Skerratt LF. 2016. History and recent progress on chytridiomycosis in amphibians. Fungal Ecology 19:89–99.

30. Piotrowski JS, Annis SL, Longcore JE. 2004. Physiology of Batrachochytrium dendrobatidis, a chytrid pathogen of amphibians. Mycologia 96:9–15.

31. Hoyt JR, Kilpatrick AM, Langwig KE. 2021. Ecology and impacts of white-nose syndrome on bats. Nat Rev Microbiol 19:196–210.

32. Verant ML, Boyles JG, Waldrep W, Wibbelt G, Blehert DS. 2012. Temperature-Dependent Growth of Geomyces destructans, the Fungus That Causes Bat White-Nose Syndrome. PLoS One 7:e46280.

33. O’Shea TJ, Cryan PM, Cunningham AA, Fooks AR, Hayman DTS, Luis AD, Peel AJ, Plowright RK, Wood JLN. 2014. Bat Flight and Zoonotic Viruses. Emerg Infect Dis 20:741–745.

Image Citations

Image sources: 

Nosferatu: A Symphony of Horror (film, 1922), via CNET

pngimg.com (URL: https://pngimg.com/image/62986)

Charter Medical (URL: https://chartermedical.com/wp-content/uploads/2017/08/T3106_blood-transfer-bags-blood-man_500x500.png)

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