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Chronic HCV treatment with peginterferon-ribavirin and severe tuberculosis re-activation


Tuberculosis (T) may be reactivated following a primary, silent, and unknown T infection, when immunodeficiency (often jatrogenic in origin), or other risk factors (e.g. cancer, cachexia), become apparent. Post-primary T episodes were described also decades after a primary M. tuberculosis infection, in patients (p) who show apparently limited radiographic signs at chest X-ray. Some grade of immunodeficiency may also depend on the administration of associated IFN-ribavirin for an underlying chronic HCV hepatitis, as expressed by the frequent emerging of leuko-neutropenia, and altered cytokine network.


In a p aged >50 years with negative history of T, an occasional chest X-ray showed fibrous-calcified infiltrates at upper right lobe. After 11 years, due to a progressive chronic HCV hepatitis, pegylated IFN-ribavirin were started for 7 months, until a sudden occurrence of cough-hemoptisis associated with a pulmonary lesion highly suggestive of T became apparent, in the same area where some reliquates of a primary T were demonstrated 11 years before.


A HRCT examination pointed out 2 different excavated infiltrates. Both direct microscropy and culture of sputum-BAL proved positive for M. tuberculosis (susceptible to all tested compounds), while Mantoux-Quantiferon assays also tested positive. An absolute lymnphopenia (nadir 966 cells/μL), prompted a T-cell subset study, which showed an imbalance of the CD4/CD8 ratio (30/45%), and an absolute CD4 count of 290 cells/μL. Notwithstanding 7 consecutive weeks of isoniazide, ethambutol, rifampicin and pyrazinamide administration, sputum examination remained positive, thus confirming the role of immunodeficiency is prompting a difficult-to-treat T. The adjunct of levofloxacin-amikacin-linezolid attained clinical-bacteriological cure, after 12 weeks.


Waiting for human experimental data, two animal models demontrated that an increased release of immunosuppressive cytokines (IL-10-TGF-β), may prompt T reactivation, while a maintained T-cell competence enhances T latency. Although a few cases of non-infectious lung involvement, interstitial pneumonia, and bronchiolitis obliterans were described during IFN therapy administered to transplant p, reactivated T was excepional. The expected increase of therapeutic use of IFN and potent agents for the management of chronic hepatitis or other diseases, might support the reactivation of latent T. A careful medical history, Mantoux reaction, IGRA testing, and a chest X-ray, are mandatory before starting IFN therapy. In fact, the jatrogenic immunosuppression related to IFN-ribavirin may go beyond the expected leuko-lymphopenia, and also act against the quantitative-functional role of CD4 lymphocytes. This last circumstance may play a key role in T reactivation, when T latency is of concern.

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Correspondence to Roberto Manfredi.

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Open Access This article is published under license to BioMed Central Ltd. This is an Open Access article is distributed under the terms of the Creative Commons Attribution 2.0 International License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Manfredi, R., Calza, L. Chronic HCV treatment with peginterferon-ribavirin and severe tuberculosis re-activation. Retrovirology 7 (Suppl 1), P83 (2010).

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