Amplification of herpes simplex virus resistance in mouse neuroblastoma (Cl300) cells

The herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) is abundantly expressed in latently infected sensory neurons. In small animal models of infection, expression of the first 1.5 kb of LAT coding sequences is necessary and sufficient for wild-type reactivation from latency. The ability of LAT to inhibit apoptosis is important for reactivation from latency. Within the first 1.5 kb of LAT coding sequences and LAT promoter sequences, additional transcripts have been identified. For example, the anti-sense to LAT transcript (AL) is expressed in the opposite direction to LAT from the 5′ end of LAT and LAT promoter sequences. In addition, the upstream of LAT (UOL) transcript is expressed in the LAT direction from sequences in the LAT promoter. Further examination of the first 1.5 kb of LAT coding sequences revealed two small ORFs that are anti-sense with respect to LAT (AL2 and AL3). A transcript spanning AL3 was detected in productively infected cells, mouse neuroblastoma cells stably expressing LAT and trigeminal ganglia (TG) of latently infected mice. Peptide-specific IgG directed against AL3 specifically recognized a protein migrating near 15 kDa in cells stably transfected with LAT, mouse neuroblastoma cells transfected with a plasmid containing the AL3 ORF and TG of latently infected mice. The inability to detect the AL3 protein during productive infection may have been because the 5′ terminus of the AL3 transcript was downstream of the first in-frame methionine of the AL3 ORF during productive infection.

Download Full-text

Herpes simplex virus latency in a hyperresistant clone of mouse neuroblastoma (Cl300) cells

Archives of Virology ◽

10.1007/bf01309927 ◽

1985 ◽

Vol 83 (3-4) ◽

pp. 319-325 ◽

Cited By ~ 9

Author(s):

Eva Nilheden ◽

S. Jeansson ◽

A. Vahlne

Keyword(s):

Herpes Simplex Virus ◽

Herpes Simplex ◽

Virus Latency ◽

Mouse Neuroblastoma ◽

Simplex Virus

Download Full-text

Effect of dexamethasone on herpes simplex virus replication in mouse neuroblastoma cells (NB41 A3): Receptor characteristics

Journal of Clinical Laboratory Analysis ◽

10.1002/jcla.1860030408 ◽

1989 ◽

Vol 3 (4) ◽

pp. 236-243 ◽

Cited By ~ 5

Author(s):

Larry L. Dreyer ◽

Robert J. Sydiskis ◽

Nasir Bashirelahi

Keyword(s):

Herpes Simplex Virus ◽

Herpes Simplex ◽

Virus Replication ◽

Neuroblastoma Cells ◽

Mouse Neuroblastoma ◽

Simplex Virus

Download Full-text

Herpes Simplex Virus Resistance and Sensitivity to Phosphonoacetic Acid

Journal of Virology ◽

10.1128/jvi.22.3.848-848.1977 ◽

1977 ◽

Vol 22 (3) ◽

pp. 848-848

Keyword(s):

Herpes Simplex Virus ◽

Herpes Simplex ◽

Virus Resistance ◽

Phosphonoacetic Acid ◽

Simplex Virus

Download Full-text

Herpes Simplex Virus Resistance to Acyclovir and Penciclovir after Two Decades of Antiviral Therapy

Clinical Microbiology Reviews ◽

10.1128/cmr.16.1.114-128.2003 ◽

2003 ◽

Vol 16 (1) ◽

pp. 114-128 ◽

Cited By ~ 252

Author(s):

Teresa H. Bacon ◽

Myron J. Levin ◽

Jeffry J. Leary ◽

Robert T. Sarisky ◽

David Sutton

Keyword(s):

Herpes Simplex Virus ◽

Herpes Simplex ◽

Antiviral Therapy ◽

Virus Resistance ◽

Host Factors ◽

Nucleoside Analogues ◽

Resistant Virus ◽

The Past ◽

Simplex Virus ◽

Virus Isolates

SUMMARY Acyclovir, penciclovir, and their prodrugs have been widely used during the past two decades for the treatment of herpesvirus infections. In spite of the distribution of over 2.3 × 106 kg of these nucleoside analogues, the prevalence of acyclovir resistance in herpes simplex virus isolates from immunocompetent hosts has remained stable at approximately 0.3%. In immuncompromised patients, in whom the risk for developing resistance is much greater, the prevalence of resistant virus has also remained stable but at a higher level, typically 4 to 7%. These observations are examined in the light of characteristics of the virus, the drugs, and host factors.

Download Full-text