Do viral infections aggravate your rheumatoid arthritis?  
By K. Molnar-Kimber, Ph.D.

Infections with the following viruses may initiate or aggravate arthritis-like symptoms, including rheumatoid arthritis in some people [1, 2].  

Please note that most people without RA can become infected with one of these viruses and not develop arthritic symptoms.  

Unfortunately, RA patients get serious infections more often than people their age.

Chronic Hepatitis C virus (HCV) infection

Chronic Hepatitis C virus (HCV) infection may lead to arthritic symptoms similar to RA in 2% to 20% of patients [3, 4].  Chronic hepatitis C infected patients with arthritis often develop rheumatoid factor (50-80% RF+) but most remain anti-CCP negative [5]. People with chronic HCV infection and arthritis symptoms often develop fibromyalgia [5] 

Clinical arthritic symptoms of chronic hepatitis C infection can mimic rheumatoid arthritis [3].  A blood test for anti-keratin antibodies can help distinguish between the two diseases in at least some patients. Most RA patients (64%) have anti-keratin antibodies, but few patients with HCV-related arthritis (9%) have them.   

The frequency of HCV infection in RA patients, however, was low in some populations [6].

Epstein Bar Virus and other viruses in Herpes family

Epstein Bar Virus has been observed in significantly higher frequency in RA patients than healthy controls [7].   T cells that kill EBV-infected cells were detected in the affected joints (synovial fluid) in RA and other inflammatory arthritis patients. In contrast, a different set of T cells that killed flu-infected cells were not there [8] 

These data suggest that EBV infections may contribute to RA symptoms in some patients.

Human Herpes Virus Type 6. RA populations have a higher rate of Human Herpes Virus Type 6 infection than healthy controls. [7].  

Cytomegalovirus has been detected in the synovial tissue of rheumatoid arthritis patients [9, 10].  Cytomegalovirus infection or reactivation appears to be associated with greater joint damage in RA patients [2].    

Herpes simplex viruses types I and II.  DNA from herpes simplex viruses was found in the synovial fluid of about one third of RA patients [11].  Persistence was associated with chronic inflammation in early RA patients.[12]   T cells that kill cells infected with herpes were found in the joint fluids of some RA patients and may aggravate RA symptoms [12].

Parvovirus B-19 infection

B19 infection is significantly higher in RA patients, especially those that carry the most common gene associated with RA: HLA-DR4 haplotype or shared epitope [13].

In one study, viral B19 DNA was detected in the synovial fluid of 25% of RA patients (8/31) [14].  Although the sample size was too small, 2 of 3 patients with early synovitis and evidence of B19 DNA, IgG and IgM subsequently developed RA.  The other patient subsequently developed SLE [14].    

Eleven of 130 early arthritis patients (8.5%) had a recent infection with B-19 virus.[15] Their symptoms included acute arthritis in several to many small joints in a symmetrical pattern—same joints on both hands or both feet.[15]   The inflammatory markers were usually low (C-reactive protein and sedimentation rate).[15]  Most patients were free of disease within 3 months.[15] 

Most early arthritis patients (73%) had had a previous B-19 infection but had not developed arthritic symptoms at the time of B-19 infection.[15]   

Some clinicians did not find a correlation between RA and B19 [16, 17]  or found the percentage of patients with B19 to be lower [18].

Hepatitis B vaccine and rheumatoid arthritis

People who received Hepatitis B vaccination had an 18 fold higher risk of developing rheumatoid arthritis in several case control studies that examined the vaccine adverse events reporting system database [19].  Hepatitis B vaccination also increased the risk for developing several other autoimmune diseases including multiple sclerosis, optic neuritis, vasculitis, arthritis, alopecia, lupus erythematosus, and thrombocytopenia. In comparison, people who received the Tetanus Control Vaccine did not develop autoimmune disease at an higher incidence [19] 

However, Ray et al reported that diagnosis of RA was not significantly higher in patients (ages from 15 to 59 years) who had been recently vaccinated with HBV (within 3 months, 6 months or 1 year) in the California Kaiser Permanente Northern California database [20]. Unfortunately Ray et al [20] did not include older patients although the maximum incidence of RA occurs in patients of 65 to 74 years [21]. Unfortunately, RA diagnosis can take longer than one year after symptoms appear in a patient.  The average time from appearance of symptoms to diagnosis in the US ranged from 3.1 years to 4.5 years [22]  

Relatives of RA patients should consider discussing the risk of being exposed to Hepatitis B virus (vaccine is often effective) in their situation, and the risk of an adverse reaction to the vaccine with their healthcare provider before obtaining it.


Infections with one or more of these viruses may be associated or aggravating your RA. 

Viral proteins or DNA in the joint tissues may induce and increase inflammation.  Some viruses are found together in about 10% of RA cases [9].    

Some people with early arthritic symptoms had a recent B-19 virus infection, and they will likely be symptom-free within three months [15].    

These data also suggest that “(a) defects in cellular immunity in patients with RA may result in a relatively high viral load; or (b) patients with RA may be more prone to infection / reactivation,” concludes Alvarez-Lafuente [7].


1.    Washing your hands with regular soap and hot water is one of the best defenses for blocking viral infections, including flu and colds. 

2.    Getting adequate vitamin D from sunshine, foods, or supplements can help maintain a balanced immune system.


3.    Enjoying five to ten servings of colorful vegetables and fruits daily can help maintain a healthy immune system and can help neutralize any toxins.  

Selected references


1.         Franssila, R.,  K. Hedman Infection and musculoskeletal conditions: Viral causes of arthritis. Best Pract Res Clin Rheumatol, 2006. 20(6): 1139-57.

2.         Pierer, M., K. Rothe, D. Quandt, et al. Association of anticytomegalovirus seropositivity with more severe joint destruction and more frequent joint surgery in rheumatoid arthritis. Arthritis Rheum., 2012. 64(6): 1740-9.

3.         Ramos-Casals, M.,  J. Font Extrahepatic manifestations in patients with chronic hepatitis C virus infection. Curr. Opin. Rheumatol., 2005. 17(4): 447-55.

4.         Rosner, I., M. Rozenbaum, E. Toubi, et al. The case for hepatitis C arthritis. Semin. Arthritis Rheum., 2004. 33(6): 375-87.

5.         Lormeau, C., G. Falgarone, D. Roulot, et al. Rheumatologic manifestations of chronic hepatitis C infection. Joint Bone Spine, 2006. 73(6): 633-8.

6.         Maillefert, J.F., G. Muller, G. Falgarone, et al. Prevalence of hepatitis C virus infection in patients with rheumatoid arthritis. Ann. Rheum. Dis., 2002. 61(7): 635-7.

7.         Alvarez-Lafuente, R., B. Fernandez-Gutierrez, S. de Miguel, et al. Potential relationship between herpes viruses and rheumatoid arthritis: analysis with quantitative real time polymerase chain reaction. Ann. Rheum. Dis., 2005. 64(9): 1357-9.

8.         Tan, L.C., A.G. Mowat, C. Fazou, et al. Specificity of T cells in synovial fluid: high frequencies of CD8(+) T cells that are specific for certain viral epitopes. Arthritis Res, 2000. 2(2): 154-64.

9.         Mehraein, Y., C. Lennerz, S. Ehlhardt, et al. Latent Epstein-Barr virus (EBV) infection and cytomegalovirus (CMV) infection in synovial tissue of autoimmune chronic arthritis determined by RNA- and DNA-in situ hybridization. Mod. Pathol., 2004. 17(7): 781-9.

10.       Stahl, H.D., B. Hubner, B. Seidl, et al. Detection of multiple viral DNA species in synovial tissue and fluid of patients with early arthritis. Ann. Rheum. Dis., 2000. 59(5): 342-6.

11.       Burgos, R., G. Ordonez, J. Vazquez-Mellado, et al. Occasional presence of herpes viruses in synovial fluid and blood from patients with rheumatoid arthritis and axial spondyloarthritis. Clin. Rheumatol., 2015. 34(10): 1681-6.

12.       Scotet, E., M.A. Peyrat, X. Saulquin, et al. Frequent enrichment for CD8 T cells reactive against common herpes viruses in chronic inflammatory lesions: towards a reassessment of the physiopathological significance of T cell clonal expansions found in autoimmune inflammatory processes. Eur. J. Immunol., 1999. 29(3): 973-85.

13.       Chen, Y.S., P.H. Chou, S.N. Li, et al. Parvovirus B19 infection in patients with rheumatoid arthritis in Taiwan. J. Rheumatol., 2006. 33(5): 887-91.

14.       Caliskan, R., S. Masatlioglu, M. Aslan, et al. The relationship between arthritis and human parvovirus B19 infection. Rheumatol. Int., 2005. 26(1): 7-11.

15.       Mauermann, M., K. Hochauf-Stange, A. Kleymann, et al. Parvovirus infection in early arthritis. Clin. Exp. Rheumatol., 2016. 34(2): 207-13.

16.       Peterlana, D., A. Puccetti, R. Beri, et al. The presence of parvovirus B19 VP and NS1 genes in the synovium is not correlated with rheumatoid arthritis. J. Rheumatol., 2003. 30(9): 1907-10.

17.       Seishima, M., Z. Oyama,  M. Yamamura Two-year follow-up study after human parvovirus B19 infection. Dermatology, 2003. 206(3): 192-6.

18.       Meyer, O. Parvovirus B19 and autoimmune diseases. Joint Bone Spine, 2003. 70(1): 6-11.

19.       Geier, D.A.,  M.R. Geier A case-control study of serious autoimmune adverse events following hepatitis B immunization. Autoimmunity, 2005. 38(4): 295-301.

20.       Ray, P., S. Black, H. Shinefield, et al. Risk of rheumatoid arthritis following vaccination with tetanus, influenza and hepatitis B vaccines among persons 15-59 years of age. Vaccine, 2011. 29(38): 6592-7.

21.       Myasoedova, E., C.S. Crowson, H.M. Kremers, et al. Is the incidence of rheumatoid arthritis rising?: results from Olmsted County, Minnesota, 1955-2007. Arthritis Rheum., 2010. 62(6): 1576-82.

22.       Molina, E., I. Del Rincon, J.F. Restrepo, et al. Association of socioeconomic status with treatment delays, disease activity, joint damage, and disability in rheumatoid arthritis. Arthritis Care Res (Hoboken), 2015. 67(7): 940-6.