Publications

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Bharat Jasani, BSc, PhD, MBChB, FRCPath. Qualifying with honours in Biochemistry (University of Glasgow,1965-1969), PhD in Experimental Pathology and MBChB (honours distinction in Pathology) (University of Birmingham, 1970-1973), Dr Jasani initiated his clinical and research training in Histopathology, at Wales National School of Medicine in 1977, achieving MRCPath (1989), FRCPath (1997), and a Specialist Consultant’s status in Histopathology (Immunohistochemistry) (1993); and Personal Chair in Oncological Pathology (2003).

We use cookies to make sure that our website works properly, as well as some ‘optional’ cookies to personalise content and advertising, provide social media features and analyse how people use our site. By accepting some or all optional cookies you give consent to the processing of your personal data, including transfer to third parties, some in countries outside of the European Economic Area that do not offer the same data protection standards as the country where you live.

Background A key challenge in the understanding and treatment of depression is identifying cell types and molecular mechanisms that mediate behavioral responses to antidepressant drugs. As treatment responses in clinical depression are heterogeneous, it is crucial to examine treatment responders and nonresponders in preclinical studies.

The molecular mechanisms underlying the clinical manifestations of COVID-19 and what distinguishes them from common seasonal influenza virus and other lung injury states such as Acute Respiratory Distress Syndrome, remains poorly understood. To address these challenges, we combine transcriptional profiling of 646 clinical nasopharyngeal swabs and 39 patient autopsy tissues to define body-wide transcriptome changes in response to COVID-19.

Recent outbreaks of Ebola virus linked to chains of transmission from the 2014-2016 West African Ebola virus epidemic suggest a new paradigm for persistent Ebola virus infections as a lasting concern to public health. Cases of Ebola virus disease linked to sexual transmission and detection of Ebola virus in the male reproductive tract long after patients have recovered suggests that Ebola virus persistence occurs in this immune privileged area. However, little is known about Ebola virus cell tropism, viral kinetics, and host response to infection in the testis.

_Demodex_ mites are obligate commensal parasites of hair follicles (HF) in mammals.  Normally asymptomatic, inflammatory outgrowth of mites can accompany malnutrition, immune dysfunction and aging, but mechanisms restricting _Demodex_ outgrowth and pathogenesis are not defined.

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Despite the development and deployment of antibody and vaccine countermeasures, rapidly-spreading SARS-CoV-2 variants with mutations at key antigenic sites in the spike protein jeopardize their efficacy. The recent emergence of B.1.1.529, the Omicron variant1,2, which has more than 30 mutations in the spike protein, has raised concerns for escape from protection by vaccines and therapeutic antibodies. A key test for potential countermeasures against B.1.1.529 is their activity in pre-clinical rodent models of respiratory tract disease.

Modern combination antiretroviral therapy (ART) regimens provide abiding viral suppression for most individuals infected with human immunodeficiency virus (HIV). However, the persistence of viral reservoirs ensures that eradication of HIV-1 (i.e., cure) or sustained ART-free remission (i.e., functional cure) remains elusive, necessitating continual, strict ART adherence and contributing to HIV-1-related comorbidities.