Local viral replication1-151 | NS1 cytotoxicity1-152 | Immune complex deposition1-154 | Erythroblast apoptosis1-160 | Autoantibody production1-164 | Cytokine upregulation1-161 | Persistence1-163 | References | |
Clinical syndromes commonly associated with B19 infection1-150 | ||||||||
TAC | + | + | 14, 40, 46 | |||||
EI | + | + | + | + | 14, 33, 44, 45 | |||
Hydrops fetalis | + | + | 48, 55 | |||||
Arthralgia/arthritis | ? | + | ? | ? | 13, 33, 46, 52, 71 | |||
Chronic PRCA | + | + | + | 14, 47, 81 | ||||
Clinical syndromes less commonly associated with B19 infection1-150 | ||||||||
Skin eruptions | + | + | ? | ? | + | 13, 33, 45, 46, 62, 85 | ||
Aplastic anaemia/cytopenias | + | + | + | + | + | 13, 14, 72, 155, 158 | ||
Hepatitis | + | 79 | ||||||
Encephalopathy/meningitis | + | 169, 173–176 | ||||||
Peripheral neuropathy | + | 53, 54 | ||||||
CFS | ? | + | 13, 59, 86, 184–187 | |||||
RA | + | + | + | + | 13, 49, 62, 82 | |||
SLE | + | + | ? | + | 61, 111, 230–238 | |||
Vasculitis | + | ? | ? | ? | + | 220–227 |
↵1-150 TAC = transient aplastic crisis; EI = erythema infectiosum; PRCA = pure red cell aplasia; CFS = chronic fatigue syndrome; RA = rheumatoid arthritis; SLE = systemic lupus erythematosus.
↵1-151 Local B19 replication occurs primarily in the erythroblasts, but also occurs in macrophages, myeloid cells, lymphocytes, hepatocytes, and dendritic epidermal and endothelial cells.
↵1-152 B19 NS1 cytotoxicity is thought to account for haematological abnormalities in EI and cytopenias and possibly for arthralgia/arthritis.
↵1-154 Immune complex deposition is thought to account for the rash of EI, arthralgia, peripheral neuropathy and may contribute to other B19 associated skin rashes and vasculitis.
↵1-160 Erythroblast apoptosis, mediated by the NS1 protein, occurs in TAC, EI, and hydrops fetalis and probably also in PRCA and aplastic anaemia/cytopenias.
↵1-164 Anti-B19 VP1 IgG cross reacts with collagen II and keratin, which may be significant in the pathogenesis of arthritis/RA and skin pathology, respectively. Antiphospholipid antibodies occur after B19 infection and may be important in the pathogenesis of symptoms which mimic SLE.
↵1-161 Upregulation of human IL6, mediated by the NS1 protein, may be important in aplastic anaemia/cytopenias and B19 associated RA; possibly also in B19 arthritis, B19 associated skin rashes, and B19 associated CFS.
↵1-163 Persistence of B19 is important in PRCA, may be important in B19 associated skin rashes, arthritis, CFS, RA, SLE, and vasculitis.