Pathogenesis Of Severe Neutropenia Research Articles

Pathogenesis of Severe Neutropenia in Patients With Primary Human Herpesvirus 6B Infection.

Although myelosuppression caused by human herpesvirus 6B (HHV-6B) reactivation in transplant recipients has been extensively investigated, the pathophysiological mechanisms of severe neutropenia in primary HHV-6B infection remain unclear. Fifty-four patients with primary HHV-6B infection were evaluated. Hematological examinations and blood sampling were conducted on days 1-4 (pre) and 5-10 (post) after the onset of illness. Severe neutropenia was defined as a neutrophil count less than 500 cells/μL. Patient characteristics, clinical data, and cytokines and chemokines levels were compared between the patients with (n = 16) and without (n = 38) severe neutropenia. Severe neutropenia was detected in samples that were collected between days 5 and 10 after illness. Significantly lower platelet counts (pre, P = 0.048; post, P = 0.032) and regulated on activation, normal T cell expressed and secreted levels (post, P = 0.007) were detected in the patients with neutropenia. Aspartate aminotransferase levels (P = 0.008), and interferon γ-inducible protein-10 (P < 0.0001), monocyte chemoattractant protein-1 (P = 0.005), and monokine induced by interferon γ (P = 0.011) levels were significantly higher in post samples collected from the patients with neutropenia. No differences were observed in any patient characteristics and serum cytokines levels. No bacterial infections were detected during the observation period. Chemokines may play an important role in the pathogenesis of severe neutropenia in patients with primary HHV-6B infection.