Host adaptation is a key factor contributing to the emergence of new bacterial, viral and parasitic pathogens. Many pathogens are considered promiscuous because they cause disease across a range of host species, while others are host-adapted, infecting particular hosts. Host adaptation can potentially progress to host restriction where the pathogen is strictly limited to a single host species and is frequently associated with more severe symptoms.
View Article and Find Full Text PDFThe late Nobel Laureate Sir Peter Medawar once memorably described viruses as 'bad news wrapped in protein'. Virus assembly in HIV is a remarkably well coordinated process in which the virus achieves extracellular budding using primarily intracellular budding machinery and also the unusual phenomenon of export from the cell of an RNA. Recruitment of the ESCRT system by HIV is one of the best documented examples of the comprehensive way in which a virus hijacks a normal cellular process.
View Article and Find Full Text PDFIt is recognized that iron overload is associated with excess mortality in HIV/AIDS, and that this may be due to iron acting as an HIV-1 transcriptional activator. In vitro evidence using iron chelators suggests that therapeutic iron depletion may be beneficial in HIV-1 infection. We describe the clinical course of a Caucasian man with hereditary haemochromatosis and HIV infection where a significant drop in HIV viral load accompanied venesection over an 18-month period in the absence of HAART.
View Article and Find Full Text PDFIntroduction: Herpes simplex encephalitis is a potentially lethal infection that should be recognised as soon as possible. The combination of clinical history and examination, brain computed tomography or magnetic resonance imaging and lumbar puncture has been used to establish a diagnosis.
Case Presentation: We present a patient who had a suggestive history but a totally normal lumbar puncture and only evidence of intracerebral haemorrhage in the brain magnetic resonance imaging.
One of the cellular defenses against virus infection is the silencing of viral gene expression. There is evidence that at least two gene-silencing mechanisms are used against the human immuno-deficiency virus (HIV). Paradoxically, this cellular defense mechanism contributes to viral latency and persistence, and we review here the relationship of viral latency to gene-silencing mechanisms.
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