The Good Housekeeper: GBV-C Co-infection with HIV

I know that the study of infectious diseases seems grim. Bacteria are increasingly becoming antibiotic resistant, baby parasites nest in your brain and tuberculosis spreads to your toes. I get it – all this devotion to the study of what gruesome-thing-du-jour is in your blood and saliva isn’t sunshine, puppies and rainbows. So in the interests of maintaining public optimism, I offer you GBV-C, a virus that has been found to offer a protective, antiviral effect against HIV infection. Yes, that HIV.

GBV-C is a member of the Flaviviridae family of viruses; a truly distinguished and deadly lot that includes hepatitis C, yellow fever, West Nile virus, dengue and a slew of nasty encephalitis-causing viruses that roost in mosquitoes and ticks. GBV-C, however, appears to exist within the body as a benign, harmless infection. It provokes no identifiable clinical symptoms of disease and seems to be the black sheep of the noxious Flaviviridae family (2).

The one thing that makes this virus notable, even outstanding!, is that for those who are co-infected with HIV and GBV-C have been shown to live significantly longer than those without GBV-C (3). If HIV is an unwelcome houseguest in the human body, then infection with GBV-C is like waking up one day and unexpectedly finding a housekeeper doing the dirty dishes and containing the mess created by this destructive guest.

A model showing the morphology of the GBV-C virus. The human body’s antibody to the E2 envelope glycoprotein may assist in stymieing HIV infection. Source: the Physician Research Network. Click for source.

GBV-C is spread in ways similar to the transmission of HIV: through sex, birth and blood. Human infection with this virus is common, with 1–8% of healthy blood donors showing evidence of infection worldwide (1). So common in fact that isolated indigenous populations in Papua New Guinea have been found to harbor the virus (3). The global distribution and evolution of the major genotypes of this virus echoes human migration patterns, indicating that this is one old viral dude that’s been hitchhiking along with humans for millions of years (3).

GBV-C provides a beneficial, antiviral effect by stymieing HIV’s advances into immune cells and spurning its replication efforts in the body. It does so in a dizzying number of ways (reader beware: it’s gonna get molecular up in here). The infection stimulates messenger signals known as cytokines to activate a cellular response and consume HIV infected cells (otherwise known as the T helper 1 (Th1) cellular response system). The virus also encourages the innate immune response by boosting pathogen-fighting interferons; this innate response can be considered one of the “first responders” of the immune system as it responds to nearly every type of infection while also activating the more advanced components of the immune system to respond to any bacterial/viral/protozoal invaders.

GBV-C stops the human cells that HIV infects, CD4+ T cells, from killing themselves in the programmed-cell-death process known as apoptosis. Apoptosis is induced by HIV-infected T cells and can affect uninfected and infected cells alike; GBV-C protects these cells maintaining their population levels. This discovery is particularly noteworthy as a crash in the population of CD4+ T cells (“CD4+ counts”) is a hallmark of immune deficiency and disease progression from HIV to AIDS.

On the left, a T cell is covered in budding HIV virus particles and will soon undergo programmed-cell-death or apoptosis. On the right, a close-up of the budding virions. Infection with GBV-C may halt this process and prevent a population crash in the numbers of CD4+ cells. Image source: Roingeard P & Brand D (1998) Budding of Human Immunodeficiency Virus. N Engl J Med. 339(32). Click for source.

The GBV-C virus causes a decrease in the cellular presence of the receptors that HIV uses to gain entry into the cell (in science speak: there’s a down-regulation of the CCR5 and CXCR4 chemokine receptors); this is akin to temporarily removing the doors of your house to predators and thieves instead of just locking them shut. In addition, GBV-C infection seems to decrease the presentation of special “activation markers” on the surface of  T cells, interfering with signaling pathways that activate the production of T cells (2). Unfortunately, it’s not entirely clear what effect this “reduced immune activation” has on the immune system and whether this assists or hinders the immune system’s response to HIV infection. Certain proteins produced by GBV-C also inhibit HIV replication (1)(3).

Overall, co-infection with the two viruses leads to increased survival of HIV-infected patients and decreased mortality (1). Not too shabby! How it does this is largely uncertain – is it due to the presence of GBV-C virus particles (known as viremia) or the body’s response to GBV-C infection and its concomitant production of antibodies against the GBV-C virus (namely the anti–GBV-C envelope glycoprotein (E2) antibody)? The fact that 15-43% of HIV-positive people show active GBV-C infection and that another 31-55% show evidence of previous infection makes it difficult to disentangle these two questions (1). However, by all accounts, what we have here looks like a symbiotic relationship between GBV-C and humans.

Two researchers behind most of the work into GBV-C have suggested that this delightful house keeper may more accurately be called the “good boy virus”, a phrase that heartily captures its place in a HIV-positive body (2). The Flaviviridae family needs all the good PR it can get and this GBV-C do-gooder might be the trick.

Though it’s unlikely HIV physicians are going to start recommending GBV-C infection to HIV-infected patients anytime soon, the work of this benign virus has intriguing implications for future virology research. Study of the virus’s housekeeping efforts may yield new targets for anti-HIV medications and alternative avenues for future research. Perhaps this virus could even be genetically-modified to magnify its HIV-fighting ways and be employed as a form of HIV treatment? We already do the opposite of this with many virulent pathogens, using weak or killed viruses as vaccines, and there are physicians out there that advocate for the use of bacteria-killing viruses; using bacteriophages to fight stubborn infections was an especially popular treatment in Eastern Europe and the former Soviet Union in the 1950s (4). In the face of mounting antibiotic resistance across the globe, using do-gooder viruses like GBV-C may soon be the only option we have left.

Resources

The United State’s FDA does not screen donated blood for GBV-C. Dozens of studies have failed to find any link whatsoever between GBV-C infection and disease and, as such, an estimated 1000 Americans a day receive blood with GBV-C virions or antibodies (2). I covered blood screening for infectious diseases in this article here.

The Phage Therapy Center in the Republic of Georgia is the pioneer in providing bacteriophage treatment for a smorgasbord of bacterial infections.

A 2006 review looks at natural resistance to HIV in certain individuals, whether that be from GBV-C, the host immune response or host genetics. It’s free!

References
1. Xiang J et al. (2004) Inhibition of HIV-1 replication by GB virus C infection through increases in RANTES, MIP-1, MIP-1, and SDF-1. Lancet. 363(9426): 2040-6
2. Bhattarai N & Stapleton JT. (2012) GB virus C: the good boy virus? Trends Microbiol. 20(3):124-30
3. Polgreen PM et al. (2003) GB virus type C/hepatitis G virus: a non-pathogenic flavivirus associated with prolonged survival in HIV-infected individuals. Microbes Infect. 5(13): 1255–1261
4. Sulakvelidze A et al (2001) Bacteriophage Therapy. Antimicrob. Agents Chemother. 45(3): 649-659. Accessible here.

Polgreen, P., Xiang, J., Chang, Q., & Stapleton, J. (2003). GB virus type C/hepatitis G virus: a non-pathogenic flavivirus associated with prolonged survival in HIV-infected individuals Microbes and Infection, 5 (13), 1255-1261 DOI: 10.1016/j.micinf.2003.08.006

Buzz Kill: Blood-Borne Disease Transmission at the Hajj

With Hanukkah and Christmas just recently past and Chinese New Year fast approaching, it seems a suitable time to consider the topic of religious celebrations and infectious diseases, no? ‘Tis the spirit and all! I’ll be looking at one of most intriguing religious events in the world, the Islamic pilgrimage to Mecca known as the Hajj, and the special epidemiological event that accompanies it.

The Hajj is a powerfully sacred and social event for Muslims. The importance of the pilgrimage to the Saudi Arabian desert city and the communal celebration of the prophet Muhammed cannot be understated – it’s a profoundly holy journey and religious duty that every Muslim is urged to complete at least once in their lifetime. It is also unique from an epidemiological standpoint: two to three million people from 70 countries meeting in one tiny place is the siren call for respiratory, water-borne and blood-borne microbial diseases.

A Muslim praying at the Hajj with a backdop of thousands of pilgrims. Image: Hassan Ammar. Click for source.

So what does the Hajj consist of exactly? Depending on the lunar calendar, the Hajj may occur any time of the year; last year, the week-long event fell between November 4th to the 9th. The pilgrimage involves a series of performative rites that must be completed in the city of Mecca and its environs; these rites serve as a reenactment of the key historical events underpinning the birth of Islam. On the first day of the Hajj, pilgrims will walk counter-clockwise seven times around a rectangular building named the Kaaba located at the very center of Mecca. The Kaaba serves as an orientation point for Muslim prayer rituals and is considered the physical and spiritual nucleus of the Islamic religion. Pilgrims, also known as Hajjees will then run back and forth between the hills of Al-Safa and Al-Marwah a total of seven times and will end their day by drinking water from the holy Zamzam well.

A map showing the Hajj route and procession taken by pilgrims. Image: Creative Commons.

The second day is spent in vigil, praying to Allah and reciting the Quran at the granite hill of Mount Arafat, located just southeast of Mecca. The following day, pilgrims will gather in the thousands to perform a ritual enactment of the Stoning of the Devil by throwing pebbles at the three pillars of Jamarat in the small town of Mina. They then leave this area to shave their heads, perform a ritual animal sacrifice and go on to celebrate the religious holiday of Eid al-Adha. Their spiritual marathon is finally complete.

During this pilgrimage, Hajjees live in a spiritual state of purity called Ihram. Prior to entering this condition, pilgrims will ritually cleanse themselves, trim their nails and remove any unwanted body hair. From then on, men are dressed simply in two sheets of unstitched white cotton and a pair of plain sandals. Women wear the hijab, with their face and hands exposed. In this sanctified state, Hajjees are forbidden from shaving, trimming their nails, wearing scented toiletries, arguing or swearing along with a few other unbecoming behaviors.

The experience can be difficult for the heat-susceptible, agoraphobic, the frail or very young; Mecca during the Hajj is often stifling hot, humid and beyond overcrowded. Performing the rites  with millions of other people over a wide geographical area can be physically strenuous and quite exhausting. There have been several recorded cases of fatal stampedes and crowd crushes during the jam-packed Stoning of the Devil, sunstroke and heat exhaustion are not uncommon, cholera outbreaks have historically plagued pilgrims, and pneumonia, meningitis and food poisoning have repeatedly occurred. Really, it goes without saying that if millions of international travelers converge in one city for a physically active, overcrowded affair, one should consider oneself lucky not to catch a respiratory or diarrheal bug.

You certainly wouldn’t expect to come down with a blood-borne transmitted virus and nasty chronic disease.

Regrettably, that scenario may not be that unlikely for male pilgrims on the verge of exiting Ihram; contracting HIV or any of the unsavory gang of hepatitis viruses such as hepatitis B, C or D (HBV, HCV or HDV) is quite possible due to the unseemly practice of communal shaving.

A pilgrim bleeding while being shaved at the end of Ihram. Note the bare hands. Image: Unknown. Click for source.

Following the Stoning of the Devil and the completion of their religious rites, Hajjees migrate to Mina where hundreds of barbers await with razor blades to shave the scalps of male pilgrims and where women will trim a finger-length lock of hair. This last ritual seals the deal, so to speak, allowing pilgrims to compete their observance of the Hajj. Saudi officials require all barbers to be licensed though makeshift barbers still abound, waiting on roads for eager pilgrims with razors in hand (1). Pilgrims may also buddy up to shave each other’s scalps. These unlicensed barbers and pilgrims can often be found reusing unsterilized blades to communally head-shave Hajjees, a fabulous technique for transmitting blood-borne diseases (BBDs).

Indeed, physicians associated with the Saudi Arabian Field Epidemiology Training Program describe the practice of communal head-shaving at the Hajj as an ‘optimum focal setting for the spread of serious BBDs’ (2). There’s a considerable amount of hair-raising unhygienic behaviors going on – not only are unsterilized razors reused on multiple individuals, barbers often do not wear gloves, incur many abrasions on their hands and dispose of the razors improperly.

Only a few studies have looked at the demographics and practices of these barbers but they have yielded some insightful data. A study in 1999 examined 158 barbers recruited from makeshift shaving sites near Jamarat. Eight nationalities were represented but the majority stemmed from three impoverished countries – 72 from Myanmar, 27 from Egypt and 22 from Bangladesh. Most interestingly, two-thirds of the barbers worked seasonally. They were not licensed professionals, but rather opportunistic seasonal workers that had worked at the Hajj for a median of two to five years (2).

The barbers reported each shave as lasting roughly two to ten minutes (3); these rapid-fire, assembly line-like operations can increase the likelihood of accidental nicks and grazes. Twenty-one percent of barbers report using a blade more than once (3). When razors are finally disposed of 83% will discard them on a ground densely covered in shorn hair instead of in the rubbish bins provided by Saudi authorities (3). This is of crucial consequence considering the numbers of pilgrims who are barefoot or wearing sandals. The head-shaving event also occurs in a very short time-frame overall, within a few hours in a circumscribed geographical area, compounding the likelihood of a BBD swap meet.

The eye-opening video below shows some of these seasonal barbers at work.

Around 90% of male pilgrims will have their scalps closely shaved (4). And pilgrims do indeed get nicks and abrasions: two separate studies found roughly 60% of Hajjees incurred scalp cuts (5)(6). There aren’t any studies examining the incidence or rate of BBD transmission among pilgrims during the Hajj so we’re unable to know how frightful of a problem this is. But consider this: many pilgrims come from regions of the world with high endemicity of BBDs such as Pakistan, Nigeria, Egypt and Turkey (2)(3)(5). And there are barbers working at the Hajj who have tested positive for BBDs – a study conducted in 1999 found that 10% tested positive for HCV and there was a positive correlation between barbers infected with HCV and the length of time they had worked at the Hajj (5). Though the epidemiological data is thin on what could actually is going on here, we can still state with some certainty that razor recycling shouldn’t be going on.

Hepatitis viruses are patient predators. They’ll stake out on bloody scalpels, syringes and surfaces for four days (HCV) or up to a week (HBV) until an open wound allows them to slink into a new body (7). It is for this very reason that Hepatitis B was one of the most commonly acquired infections in hospitals among medical personnel before the advent of the hepatitis A/B vaccine. When razor are used frantically and repeatedly to shave pilgrim’s heads, accidents will naturally happen. Skin catches on the blade. A microscopic cut, a slight nick and a drop of blood beads. Maybe in the hubbub, in the physical and spiritual heat of the moment, a barber grazes his bare hands and fingers on that pilgrim’s blood droplet. Or accidentally smears his own fresh blood, precipitated by a slip of the blade on an earlier scalp. The blood blends, indistinguishable from the other. Was that barber or pilgrim infected; did a virus slip between the two? In any case, another eager, awaiting Hajjee sits down for a shave and the razor is used again. This happens over and over and over, until the razor blade is finally deemed blunt and useless.

A public health poster in a Saudi Arabaian hospital warning pilgrims of the dangers posed by shaving during the Hajj. Image: Uknonwn. Click for source.

It’s a perverse tragedy that pilgrims exiting a state of profound spiritual and physical holiness may find their very blood contaminated by a barber with unhygienic practices. Pilgrims can become infected with a fatal illness that is clinically asymptomatic in its early stages only to fly back home to their communities oblivious of their condition. Catching the flu or pneumonia at the Hajj is one thing but bringing home a deadly viral illness is quite another.

Clearly the provision of safe razor blades, screening and supervision of barbers and widespread education on this matter are desperately needed. In a study from 1998, 74% of Hajjees and 20% of barbers were unaware that diseases could be transmitted by used razor blades (3). Many pilgrims expressed more concern about the spread of visible skin diseases than anything else. The invisible nature of BBDs only helps to further conceal the potential for a BBD micro-epidemic at the Hajj.

Consideration of the provision of housing, sanitation and overall public health of these religious visitors is of enormous importance for Saudi Arabian officials planning for the Hajj, and they do a phenomenal super-human job of keeping millions of people safe and cared for by providing free health care, organizing the festivities and what not. Seven hospitals have been established to provide free medical services and can supply over 2000 beds for those requiring hospitalization (6). The Ministry of Health establishes infection control policies using current knowledge of ongoing global outbreaks, infectious disease epidemiology and established preventative medicine techniques (1)(5). By all accounts, they did a great job during the H1N1 flu pandemic in 2009 by requiring pilgrims to have flu shots, restricting visas for pilgrims from affected countries, setting up thermal sensors at airports to detect the feverish and deploying thousands of physicians throughout the pilgrim circuit (9). They also require all entering pilgrims to display certificates of vaccination for hepatitis A/B, meningococcal meningitis and yellow fever.

A pilgrim recieving a shave in a sanctioned barbershop during the Hajj. Image: Unknown. Click for sourece.

But keeping an eye on rogue unlicensed barbers can be difficult for officials considering the high crowd density and activity. Whatever may be the case, the seriousness of the matter can’t be ignored. A vigorous public health campaign as well as a serious crackdown on these barbers is needed in order to halt this hairy business. It’s been noted before that an epidemic of the flu, meningitis or cholera could easily bloom into a pandemic at the Hajj. Even so, the prospect of a multinational epidemic of BBDs spread by irresponsible hygiene practices is appalling. A hair-raising thought, indeed.

Recommended Reads

The hepatitis family, particularly the members B, C and D, is some real nasty shit. I didn’t go into any detail about their molecular biology but if you’re interested, please go here.

Go here to see the vaccinations required by the Saudi Ministry of Health for all visiting pilgrims.

For a list of every single conceivable disease you could catch during the pilgrimage, check out this baby.

An extremely helpful guide to how to handle oneself at the Hajj.

References

(1) ZA Memish. (2002) Infection control in Saudi Arabia: Meeting the challenge. Am J Infect Control. 30(1): 57-65
(2) The  Saudi Arabian Field Epidemiology Training Program (2000) Blood-Borne Diseases Among Barbers During Hajj, 1419 H (1999). Saudi Epidemiology Bulletin: 7(1). Accessed online on Dec 10, 2011. Link.
(3) Saudi Arabian Field Epidemiology Training Program (1998) Head-shaving practices of barbers and pilgrims to Makkah, 1998 Saudi Epidemiology Bulletin. 5(3): 18-19
(4) SM Rafiq, H Rashid, E Haworth & R Booy. (2009) Hazards of hepatitis at the Hajj. Travel Med Infect Dis. 7(4): 239-46
(5) Rashid H & Shafi S. (2006) Blood borne hepatitis at Hajj. J of Hep Mon. 6(2): 87-88
(6) Alrabeh AM, El-Bushra HE, Al-Sayed MO, et al. (1998) Behavioral risk factors for disease during Hajj: the second survey. Saudi Epidemiol Bull. 5(3). Accessed online on Dec 10, 2011. Link.
(7) CDC; Division of Viral Hepatitis. (2009) Hepatitis B FAQs for the Public. Accessed online on January 4, 2012. Link.
(8) Omar Sacirbey, 2009, Will flu epidemic slow the Hajj? Chron.com (Online). Accessed online on Dec 10, 2011. Link.

Memish ZA (2002). Infection control in Saudi Arabia: meeting the challenge. American journal of infection control, 30 (1), 57-65 PMID: 11852419

Of Warts & Men: Meat-Handlers Infected with Human Papillomavirus 7

Every profession seems to have its own tailor-made occupational hazard. Veterinarians suffer bites and scratches, office workers struggle with carpal tunnel syndrome, anxiety torments professional graduate students and so on. A few years ago, I was stunned to hear that butchers, fish-mongers and those intimately involved in the meat-handling trade (please don’t read into that any more than is necessary) are more likely to be infected with a certain strain of Human Papillomavirus (HPV). Odd, huh? And kind of gross.

A scanning electron micrograph of a negatively-stained HPV virion. Image: Unknown. Source: Laboratory of Tumor Virus Biology. Click for source.

The thriving 120-member HPV family is quite successful at infecting humans, with up to the 20% of a population infected with a HPV wart or verruca (1). This family is as familiar to the human body as the warming, joyful sensation of the sun on our skin. The viruses are real home-bodies, typically favoring one part of the body whether that be the feet, hands, anogenital region or what-have-you. The HPV family is roughly segmented into three infection subtypes: anogenital and/or mucosal, non-genital cutaneous, and epidermodysplasia verruciformis (EV), a rare, hereditary infection that can cause widespread squamous cell skin tumors (2). The papillomaviruses show strict species specificity; attempts at a Frankensteinian or “Heart of a Dog” type of cross-species viral infection have been, thankfully, unsuccessful (4).

HPV causes epithelial proliferations of the skin and mucous membranes, with a clinical expression resulting in anything from benign warts to invasive tumors. Warts are acquired by direct or indirect contact; infected individuals transmit the infection by living their life day-to-day, unknowingly smearing HPV particles on surfaces willy-nilly (5). And so we go about living our lives, blissfully unaware of such matters. Until now, that is.

The HPV family has the ignoble distinction of being the most commonly sexually transmitted disease with over 40 viruses capable of infecting the genitals, mouth and throat. It’s quite impressive, really. HPV-16 and HPV-18 are the most familiar to us, being globally ubiquitous and responsible for causing genital warts as well as the great majority of cases of cervical cancer, now easily preventable by vaccination (if people would get vaccinated, that is!).

Common warts found on the hands, palms and around the nails and plantar warts on the feet are most often caused by strains HPV-2 and HPV-4, though HPV-1 and many more may also be responsible. These verrucas  of the hands and feet typically affect children and young adults (much to the dismay of mothers). This self-limiting infection can be difficult to treat and fully eradicate – warts can either be non-responsive to or reappear after treatment. Dermatologists recommend letting them reside and proliferate benignly until the immune system kicks into high gear and eliminates them.

"Butcher's Stall" by Pieter Aertsen, 1508 - 1575. Click for source.

In 1969, a physician named Jerome Litt found that meat-handlers had a greater incidence of hand warts than the general population (3). These warts were often quite abundant, grew in a proliferative fashion and were localized to the dorsal and palmar sides of the hand (4). The warts have been described as having a cauliflower-like appearance. Hyperkeratinosis is often seen, where the outermost layer of the epidermis, the stratum corneum, has thickened and darkened. The increased prevalence of warty hands within this population remains the case today where it is estimated that up to 23% of people who frequently handle meat, fish and poultry will develop warts on their hands (5).

Initially, researchers thought the warts of those involved with the slaughtering or butchering of cows were a result of a bovine papillomavirus (BPV), seemingly infected by the virus in a direct cow-to-human transfer. It seemed reasonable enough: the warts are localized to the hands, these guys are in frequent contact with blood and flesh, ergo these verrucas are bound to be a cow wart virus. Even so, after many biopsies and running samples through PCRs, researchers have found that these viruses are all of the human variety.

In several studies of butcher’s warts, researchers have found that HPV-2, HPV-4 or HPV-7 are the most common culprits, with HPV-7 leading the pack (5). Often, several HPV subtypes have been found on one hand, throwing themselves a good ol’ warty party (7). So we have a situation in which men who work in abattoirs and retail and wholesale butcher shops were showing evidence of a profession-specific viral warty infection.

Butchers at work in 1928 at the Loch Bros. butchery in Emerald, Australia. Image: Unknown. Source: John Oxley Library. Click for source.

Even those working in the seafood industry aren’t spared. Fishmongers also can become infected with the HPV types HPV-1, HPV-2, HPV-4 and HPV-7 (8). In fact, researchers found that infection with HPV-7 was directly correlated with the length of time one had been employed as a fishmonger, a finding similar to that in the case of the abattoir and butcher workers (5). Poultry workers and farmers have also been found with infections, so this is not a bovine-specific hazard.

So why do people working exclusively in the butchering industry get this human virus while we non-meat-handling office workers and laborers are spared? The simple answer is “we don’t know”. We really don’t. The reservoir of HPV-7 and where it hides out, why meat-workers are disproportionately infected and what the role of the flesh of animals or the slaughtering environment has to do with the propagation of the virus are all frustratingly unknown.

Proliferative warts localized to the dorsal side of the hand similar to what a HPV-7 infection may look like. Image: Logical Images. Source: SkinSight. Click for source.

Some speculate that environmental conditions may well be a serious factor in HPV-7 infection (8). It has been shown that abrasions of the skin encourage penetration of the HPV virus and proliferation of common and plantar warts (5). And we know that meat-handlers typically work with a variety of animals with very sharp knives in wet and cold environmental conditions. It’s a gem of a setting: working with flailing, dying animals, surrounded by fur, blood and scales, and acquiring minor abrasions and accidental lacerations throughout. It seems quite reasonable to expect that they would get some infection or another, so why not some harmless warts?

Now the “but”: a group of British researchers have conducted extensive surveys looking at hand trauma, environmental conditions and handling of specific kinds of meat and found no association between these factors and hand wart or HPV-2 and HPV7 prevalence (6). There was also no evidence of person-to-person transmission, meaning that butchers aren’t spreading this virus to their work-mates in their working environment (7). These results suggest that HPV-7 is distributed throughout the population but only causes disease under certain environmental conditions or stimuli, and that there is some component of animal flesh that predisposes activation, infection and/or replication of HPV-7 in the epithelia (6).

In other words, there’s something in a slaughtering/butchering environment that encourages replication and growth of HPV. Does meat or blood have some sort of immunosuppressive factors that allow for HPV-7 to blossom on butchers’ hands? One study clearly seems to support this idea with the finding that lower incidences of warts are found in those working in modern slaughterhouses, with automated butchering rather than butchering by hand (5). Warts can develop within two years of working with meat, which also seems to suggest that cumulative exposure is necessary before your hands start growing some new, minor appendages (8).

Alas, the research is rather thin on HPV-7. There just isn’t that much of an academic drive for investigating this rare, benign virus that affects a sub-set of professionals. But what a good, meaty mystery, eh? Definitely something to consider when you’re deciding whether to embark on a career change as, say, the latest hipster butcher. In the meantime, take this as a cautionary tale to wash your hands frequently and especially after preparing your filet mignon for tonight’s dinner.

Resources
For more information on the molecular structure and pathogenesis of HPV, there’s a public-access PDF from 1993 that’s helpful but mostly focuses on cervical strains. This student-made page from Brown University is also insightful.

For a list of the different types of warts and the HPV strains that cause them, go to the helpful eMedicine overview.

For an catalogue of truly alarming images of warts, I reluctantly point you in the direction of the DermNet NZ site. NSFW and NSFFH (Not Safe For the Faint of Heart).

References
1) S Jabłońska, S Majewski, S Obalek, G Orth. (1997) Cutaneous Warts. Clin Dermatol. 15(3): 309-19
2) PA Gearhart. (2011) Human Papillomavirus. Medscape Reference. Retrieved: Oct 13, 2011 from http://emedicine.medscape.com/article/219110-overview
3) JJ Meffert (2001) Butcher’s Warts: Dermatological Heritage or Testable Misinformation? Arch Dermatol. 137(3): 384-5
4) W Melchers, S de Mare, E Kuitert, J Galama, J Walboomers, and AJ van den Brule. (1993) Human Papillomavirus and Cutaneous Warts in Meat Handlers. J Clin Micro. 31(9): 2547-49
5) R Rüdlinger, MH Bunney, R Grob & JA Hunter (1989) Warts in fish handlers. Br J Dermatol. 120(3):375-81
6) M Keefe, A al-Ghamdi, D Coggon, NJ Maitland, P Egger, CJ Keefe, A Carey, CM Sanders (1994) nBr J of Dermatol. (130)1: 9–14
7) M Keefe, A al-Ghamdi, D Coggon, NJ Maitland, P Egger, CJ Keefe, A Carey, CM Sanders (1994) Butchers’ warts: no evidence for person to person transmission of HPV7.  Br J of Dermatol. (130)1: 9–14
8) A Tosti & BM Pieraccini (2001) Warts of the Nail Unit: Surgical and Nonsurgical Approaches. Dermatol Surg. 27(3): 235-9

KEEFE, M., AL-GHAMDI, A., COGGON, D., MAITLAND, N., EGGER, P., KEEFE, C., CAREY, A., & SANDERS, C. (1994). Cutaneous warts in butchers British Journal of Dermatology, 130 (1), 9-14 DOI: 10.1111/j.1365-2133.1994.tb06874.x
Melchers W, de Mare S, Kuitert E, Galama J, Walboomers J, & van den Brule AJ (1993). Human papillomavirus and cutaneous warts in meat handlers. Journal of clinical microbiology, 31 (9), 2547-9 PMID: 8408588