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1.
Bioscience ; 64(7): 612-618, 2014 Jul.
Article in English | MEDLINE | ID: mdl-25561747

ABSTRACT

Achieving trainee diversity in science, technology, engineering, and mathematics is rapidly becoming a challenge faced by many nations. Success in this area ensures the availability of a workforce capable of engaging in scientific practices that will promote increased production capacity and creativity and will preserve global scientific competitiveness. The near-term vision of achieving this goal is within reach and will capitalize on the growing numbers of underrepresented minority groups in the population. Although many nations have had remarkable histories as leaders in science and technology, few have simultaneously struggled with the challenge of meeting the educational and training needs of underrepresented groups. In this article, we share strategies for building the agency of the scientific community to achieve greater diversity by highlighting four key action areas: (1) aligning institutional culture and climate; (2) building interinstitutional partnerships; (3) building and sustaining critical mass; and (4) ensuring, rewarding, and maximizing faculty involvement.

2.
J Virol ; 87(24): 13490-8, 2013 Dec.
Article in English | MEDLINE | ID: mdl-24089568

ABSTRACT

The human JC polyomavirus (JCPyV) causes the rapidly progressing demyelinating disease progressive multifocal leukoencephalopathy (PML). The disease occurs most often in individuals with AIDS but also occurs in individuals receiving immunomodulatory therapies for immune-related diseases such as multiple sclerosis. JCPyV infection of host cells requires the pentasaccharide lactoseries tetrasaccharide c (LSTc) and the serotonin receptor 5-hydroxytryptamine (5-HT) receptor 5-HT2AR. While LSTc is involved in the initial attachment of virus to cells via interactions with VP1, the mechanism by which 5-HT2AR contributes to infection is not clear. To further define the roles of serotonin receptors in infection, HEK293A cells, which are poorly permissive to JCPyV, were transfected with 14 different isoforms of serotonin receptor. Only 5-HT2 receptors were found to support infection by JCPyV. None of the other 11 isoforms of serotonin receptor supported JCPyV infection. Expression of 5-HT2 receptors did not increase binding of JCPyV to cells, but this was not unexpected, given that the cells uniformly expressed the major attachment receptor, LSTc. Infection of these cells remained sensitive to inhibition with soluble LSTc, confirming that LSTc recognition is required for JCPyV infection. Virus internalization into HEK293A cells was significantly and specifically enhanced when 5HT2 receptors were expressed. Taken together, these data confirm that the carbohydrate LSTc is the attachment receptor for JCPyV and that the type 2 serotonin receptors contribute to JCPyV infection by facilitating entry.


Subject(s)
JC Virus/physiology , Leukoencephalopathy, Progressive Multifocal/metabolism , Receptor, Serotonin, 5-HT2A/metabolism , Receptor, Serotonin, 5-HT2B/metabolism , Receptor, Serotonin, 5-HT2C/metabolism , Virus Internalization , HEK293 Cells , Humans , JC Virus/genetics , Leukoencephalopathy, Progressive Multifocal/genetics , Leukoencephalopathy, Progressive Multifocal/virology , Receptor, Serotonin, 5-HT2A/genetics , Receptor, Serotonin, 5-HT2B/genetics , Receptor, Serotonin, 5-HT2C/genetics , Serotonin/metabolism
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