Dr. Kevin A Cassady M.D.
Infectious Disease Specialist (Pediatric) | Pediatric Infectious Diseases
1600 7th Ave S Birmingham AL, 35233About
Dr. Kevin Cassady is a pediatric infectious disease specialist practicing in Birmingham, AL. Dr. Cassady specializes in recurring or persistent diseases caused by bacteria, parasites or fungus in infants, children and adolescents. Pediatric infectious disease specialists also provide consultation to other health care professionals dealing with complex cases.
Board Certification
PediatricsAmerican Board of PediatricsABP- Pediatric Infectious Diseases
Provider Details
Expert Publications
Data provided by the National Library of Medicine- Second-site mutation outside of the U(S)10-12 domain of Deltagamma(1)34.5 herpes simplex virus 1 recombinant blocks the shutoff of protein synthesis induced by activated protein kinase R and partially restores neurovirulence.
- The herpes simplex virus type 1 U(S)11 protein interacts with protein kinase R in infected cells and requires a 30-amino-acid sequence adjacent to a kinase substrate domain.
- Human cytomegalovirus TRS1 and IRS1 gene products block the double-stranded-RNA-activated host protein shutoff response induced by herpes simplex virus type 1 infection.
- Ulceroglandular tularemia in a nonendemic area.
- Acyclovir-resistant chronic verrucous vaccine strain varicella in a patient with neuroblastoma.
- Herpesvirus vectors for therapy of brain tumors.
- Strategies for the rapid construction of conditionally-replicating HSV-1 vectors expressing foreign genes as anticancer therapeutic agents.
- Spontaneous and Engineered Compensatory HSV Mutants that Counteract the Host Antiviral PKR Response.
- Δγ₁134.5 herpes simplex viruses encoding human cytomegalovirus IRS1 or TRS1 induce interferon regulatory factor 3 phosphorylation and an interferon-stimulated gene response.
- Hypoxia Moderates γ(1)34.5-Deleted Herpes Simplex Virus Oncolytic Activity in Human Glioma Xenoline Primary Cultures.
- Human herpesviridae methods of natural killer cell evasion.
- STAT1 and NF-κB Inhibitors Diminish Basal Interferon-Stimulated Gene Expression and Improve the Productive Infection of Oncolytic HSV in MPNST Cells.
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