SummaryKaposi's sarcoma-associated herpesvirus (KSHV) is the primary aetiological agent of at least three malignancies associated with HIV infection and immunosuppression: Kaposi's sarcoma, primary effusion lymphoma and multicentric Castleman's disease. KSHV encodes proteins that deregulate key checkpoints in the signalling pathways governing cell proliferation, which may ultimately contribute to the virus' oncogenic potential. To alter cellular signalling associated with proliferation, these viral proteins function like growth factor ligands/receptors, signal transduction proteins, transcription factors and cell cycle regulators. This review focuses on the mechanisms by which some KSHV-encoded proteins activate signalling pathways and cell proliferation and their role in the pathogenesis of KSHV-driven mechanisms.

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Minimal hepatic encephalopathy (mHE) is common among patients with cirrhotic liver disease and causes significant morbidity and mortality. It may present as cognitive impairment, behavioural changes and, less frequently, with neurological symptoms which make diagnosis of the disease challenging. A history of falls and accidents may also be suggestive of mHE. Diagnosis primarily relies on at least two positive psychometric tests of which the psychometric hepatic encephalopathy score (PHES) is essential. Alternatively, PHES and an electroencephalogram may be used to establish a diagnosis. Biochemical markers of encephalopathy currently have no role in the diagnosis of mHE. Treatment is not always advocated for a diagnosis of mHE but is dependent on the degree of impairment caused by the symptoms. After treatment of other metabolic abnormalities and co-morbidities associated with cirrhosis, more specific treatment for mHE largely relies on therapies used to lower ammonia levels. Laxatives and rifaximin are commonly used in treatment and work through decreasing ammonia absorption from the gut. Other therapies, such as BCAA, LOLA, L-carnitine and phenylbutyrate, modify responses to ammonia as well as enhancing metabolism and excretion. mHE resulting from spontaneous portosystemic shunts or transhepatic intraportal systemic shunts may require ablation or reduction of the shunt. Early detection and appropriate treatment of mHE is important to prevent significant cognitive impairments and progression to overt HE.