Rebeca de Paiva Fróes Rocha, Ph.D.

Research

Mycobacterium avium is a slow-growing nontuberculous mycobacterium (NTM) known for causing opportunistic infections, especially in patients with AIDS. Its rising incidence and treatment challenges have renewed attention on this pathogen. M. avium along with M. intracellulare—referred to as Mycobacterium avium complex—is the most common cause of NTM pulmonary disease worldwide. Despite the close relation to Mycobacterium tuberculosis (Mtb), NTMs employ distinct immune evasion strategies that significantly affect disease management and treatment approaches. Infections with M. avium are particularly challenging due to its antibiotic resistance and persistence within host cells. Current treatments for NTM pulmonary disease involve long, toxic chemotherapy regimens with poor cure rates, compounded by the lack of drugs specifically optimized for NTM pathogens, leading to significant side effects and compliance issues. Type I interferon (IFN-I) is one of the primary molecules induced by the immune system upon pathogen recognition. Although traditionally associated with antiviral functions, its importance in Mtb infection is highlighted by our group, particularly through the work of Stanley et al., who propose that Mtb has evolved to exploit the IFN-I response to facilitate bacterial growth, underscoring a central role for IFN-I in Mtb’s immune evasion strategies. Beyond the insights gained from Mtb, our understanding of IFN-I in other mycobacterial species remains limited. Therefore, understanding these mechanisms is crucial, as the rising incidence of M. avium and its inherent cell persistence and resistance to antibiotics present significant treatment challenges. By gaining a deeper insight into the role of IFN-I in M. avium’s pathogenesis and immune evasion strategies, the Cox lab will develop more effective treatment strategies, address challenges posed by pathogen persistence and antibiotic resistance, and ultimately improve the management of mycobacterial diseases.