Student guest post by D.F. Johnston

Many who have had the responsibility of taking care of man’s best friend hear “parvo” or “parvovirus” and their thoughts leap immediately to something Fido needed to be vaccinated for. But while there is a canine parvovirus, a human one known as parvovirus B19 also exists. Person-to-person transmission of parvovirus B19 is primarily through aerosol spread, although maternal-fetal and blood-borne spread is also possible [1]. It is important to note that B19 infection is not acquired from time spent playing fetch with Fido; the canine parvovirus and human parvovirus are species-specific [2].

In addition to asymptomatic infection or general flu-like symptoms, this single-stranded DNA virus can also cause rash (primarily in children) and, more commonly in adults, arthritis, especially in the fingers and hands but also in the wrists and ankles [1]. According to Colmegna and Alberts-Grill, 80% of adults experience joint pain from B19 infection [1] and arthritic symptoms are suffered 60% of the time in women as compared to 30% in men [3]. While most arthritis experience lasts approximately two weeks and resolves on its own, slightly less than one in five of those patients will continue to have chronic arthritis for a period ranging from months to years [1].

Interestingly, the chronic arthritis experienced following B19 infection is so similar to clinical presentation for rheumatoid arthritis (RA) that 50% of patients experiencing it meet the criteria for diagnosis of RA [4]. Difficulty in distinguishing between B19-chronic arthritis and RA is made even more difficult because interaction between B19 virus and the immune system leads to the production of several kinds of autoantibodies, including the rheumatoid factor used in diagnosis of RA [1].

The joint pain and inflammation associated with B19 is thought to be caused by multiple factors, including a viral protein that may act like a host enzyme that is involved in activation of immune-mediated inflammation [1]. One of the most significant proposed factors is molecular mimicry, where some part of the B19 virus recognized by the immune system is so similar in appearance to something in human joint tissues that the immune system mistakenly attacks joint tissue, resulting in the pain and arthritis associated with B19 infection [1]. This is an extremely important point since a similar mechanism is associated with RA and several studies found evidence of B19 infection in both patients with RA and lupus, which prompted investigations into a causal role of B19 in not just acute arthritis but RA as well as lupus [3].

Unfortunately, study results have been fairly contradictory in assessing parvovirus B19 as a causal component in RA or lupus. Some studies have tentatively suggested an association needing further investigation and others have more explicitly stated a causal role for B19 [3, 4]. Contrasted with this are several studies that conclude B19 is not a cause of RA or lupus [3, 4]. The problem with many of the studies trying to demonstrate the causal nature of B19 is that a large number focus on presence of either B19 or antibodies against B19 in people who already have the disease of interest [3, 4] which only shows that B19 and RA or lupus are both present, not that a person was first infected with B19 and then developed RA or lupus. Other studies are not even cross-sectional in nature but are case series [5] involving a small number of patients, which may be valuable for generating hypotheses but lack scientific rigor for testing the causal relationship. Given the fairly weak evidence demonstrating an association pitted against stronger data supporting no relationship, it appears that opinions generally come down on the side of either an unlikely causative role for B19 in RA or lupus [2, 3] or “inconclusive” data at this point [1]. Despite sharing the former conclusion, Naides still argues that the similarity between proposed mechanisms for B19-induced arthritis and rheumatoid arthritis leaves understanding the mechanism behind arthritis from B19 as an important method for potentially improved understanding of RA [2].

Whatever the role of parvovirus B19 in development of either rheumatoid arthritis or lupus, it does cause both acute and chronic forms of arthritis in addition to the general “flu-like symptoms” that are often encountered with infectious diseases. Despite the species-specific nature of canine and human parvoviruses, our susceptibility to B19 infection leaves us with one more experience we share with our four-legged friends.

Works Cited:

1. Colmegna, I. & N. Alberts-Grill. 2009. “Parvovirus B19: its role in chronic arthritis.” Rheum Dis Clin N Am, 35(1): 95-110.

2. Naides, S.J. “Rheumatic manifestations of parvovirus B19 infection.” Rheum Dis Clin N Am, 24(2): 375-401.

3. Moore, T.L. “Parvovirus-associated arthritis.” Curr Opin Rheumatol, 12(4): 289-94.

4. Lunardi, C., Tinazzi, E., Bason, C., Dolcino, M., Corrocher, R., & Puccetti, A. “Human parvovirus B19 infection and autoimmunity.” Autoimmun Rev, 8(2): 116-20.

5. Gran, J.T., Johnsen, V., Myklebust, G., & Nordbe, S.A. “The variable clinical picture of arthritis induced by human parvovirus B19.” Scand J Rheumatol, 24(3): 174-9.