Protective Immunity Against Cryptococcus Neoformans Infection

Abstract

Cryptococcus neoformans, the etiological agent of cryptococcosis, is an occasional opportunistic fungal pathogen of immune competent individuals. However, it is a relatively frequent cause of life-threatening meningoencephalitis and pulmonary infections in immunosuppressed hosts and is a leading mycological cause of morbidity and mortality among patients with AIDS in most parts of the world. The lack of an effective fungicidal regimen and the development of antifungal resistant strains suggest that continued investigation is necessary to devise immunotherapeutic strategies, drug targets and/or vaccines to combat C. neoformans infections. Until recently, cryptococcal virulence factors such as its polysaccharide capsule, macrophage parasitism, and its ability to induce an ineffective antibody mediated immune (AMI) response along with a non-protective type II (Th2) cell-mediated immune response have thwarted efforts to induce complete protective immunity against a lethal cryptococcal strain in murine models. The presence of C. neoformans antibodies in adult human serum suggests that immune competent individuals have difficulty resolving an early cryptococcal infection allowing for the establishment of a subclinical chronic infection. Recent studies have shown that pro-inflammatory cytokines, specifically interferon-g (IFN-g), associated with type I (Th1) cell-mediated immunity can successfully drive cell-mediated immune (CMI) responses to produce protective immunity to a second experimental C. neoformans infection in mice. This review will evaluate the intricacies of the host-cryptococcal interaction and discuss recent developments in C.neoformans research and the potential for human vaccines and/or drug therapies.

Prevalence, treatment, and factors associated with cryptococcal meningitis post introduction of integrase inhibitors antiretroviral based regimens among People Living with HIV in Tanzania

“…The infection is not transferred from person to person, but results from the inhalation of infectious spores mainly found in bird droppings, that multiply in the lungs and can spread to the membranes covering the brain and spinal cord causing meningitis [ 7 ]. In HIV-infected patients, the disease is considered as a result of recurrence of latent infection which occurs months to years after the initial exposure event [ 8 , 9 ].…”