Summary:Respiratory syncytial virus (RSV) is known to cause acute lung injury in the immunocompromised host, especially recipients of bone marrow allografts. Specific prognostic factors for the development of severe lifethreatening disease remain to be identified as does the optimum treatment of established disease. Over a 5-year period the incidence and outcome of RSV in BMT recipients was analysed retrospectively. Prognostic factors assessed included type of transplant, engraftment status at the time of infection, the presence of lower respiratory tract disease, viral genotype and treatment received. During the study period, 26 of 336 (6.3%) allogeneic stem-cell recipients were identified as having RSV. Five patients (19.2%) died as a direct result of RSV. One patient died secondary to an intracranial bleed with concomitant RSV. There were four patients with graft failure (two primary and two secondary) attributable to the presence of RSV, two of whom subsequently died of infections related to prolonged myelosuppression. The presence of lower respiratory tract infection and a poor overall outcome was the only statistically significant association. Unrelated donor transplants and AML as the underlying disease appeared to be associated with a poorer outcome. Engraftment status, viral genotype and RSV treatment received did not correlate with outcome. We conclude that future studies are required to identify early sensitive and reproducible prognostic factors of RSV in the immunocompromised host. The roles of intravenous and nebulised ribavirin need to be clarified by prospective controlled trials.

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In contrast to studies of adult oncology patients, paediatric oncology patients in our institution appear at low risk of cryptosporidiosis.

Human adenoviruses are non‐enveloped, double stranded DNA viruses responsible for many upper‐respiratory infections and eye infections. It is composed of a spherical capsid that surrounds the viral genome. The trimeric fiber protein, exposed on the capsid exterior, is unique to adenoviruses and facilitates the attachment to the host cell via interactions between the knob domain and cell surface proteins. After entry into the host the virus is carried to the nucleus, where the capsid disassociates and the DNA passes through the nuclear pore. The adenovirus is of particular interest for the role it may play in targeted gene therapy as a vector.Further study of the virus' structure, specifically the knob domain located on the fiber protein, may allow for genetic alterations to specific cell surface proteins and to circumvent neutralizing antibodies. In addition, knowledge of the structural details provides ways to disrupt their assembly and disassembly, thereby interfering with their natural lifecycle and associated infections. The structural details can also be used to re‐target the adenoviruses to the cells of interest and deliver specific genes, thus making it a useful delivery vehicle. The El Capitan SMART (Students Modeling A Research Topic) Team modeled the fiber protein using 3D printing technology. Supported by a grant from the HHMI Pre‐College Program

Viral infections are one of the leading causes of death in humans and are usually caused by the adenovirus. The early region protein (E1A) is a multifunctional protein expressed by the adenovirus and essential for transformation of the host cell, ultimately resulting in oncogenesis. Through E1A's interactions with the host cell's retinoblastoma protein (pRb) and CREB binding protein (CBP), E1A prevents natural cellular functions. Our focus is the interaction site between E1A and CBP/p300, specifically the transcriptional adaptor zinc finger‐2 (TAZ2) of CBP/p300. Upon interaction with the TAZ2 domain, E1A undergoes coupled folding, allowing it to bind with TAZ2, competing with, and inactivating, the transactivation domain (TAD) of the tumor suppressor p53. Through competition with p53, E1A is able to inhibit apoptosis and cell cycle arrest, thus causing the cell to divide uncontrollably. E1A has the ability to reprogram gene expression. Understanding the structure of the complex will help us to design a therapeutic that would prevent E1A from interacting with CBP, allowing normal interaction with p53 to occur. This will prevent cancer in association with adenovirus infection and help us to understand more about cancer‐causing viruses in general. The El Capitan High School SMART Team (Students Modeling A Research Topic) modeled E1A using 3D printing technology. Supported by a grant from HHMI Pre‐College Program