The effects of photodynamic therapy on Vero cells and replication of herpes simplex type 1: an in vitro analysis

Author(s):  
Rosângela Maria Callou Pinheiro ◽  
Maria Tereza Villela Romanos ◽  
Antonio Canabarro ◽  
Ana Cecília Aranha ◽  
Maíra Prado ◽  
...  
1993 ◽  
Vol 101 (6) ◽  
pp. 843-851 ◽  
Author(s):  
Claire Rogel-Gaillard ◽  
Gérard Pehau-Arnaudet ◽  
Françoise Breitburd ◽  
Gérard Orth

2018 ◽  
Vol 8 (2) ◽  
pp. 81-85 ◽  
Author(s):  
Abdi Hussein Hadun ◽  
James Mucunu Mbaria ◽  
Gabriel Oluga Aboge ◽  
Mitchel Otieno Okumu ◽  
Antony Letoyah Yiaile

2005 ◽  
Vol 79 (20) ◽  
pp. 12783-12797 ◽  
Author(s):  
John W. Balliet ◽  
Jonathan C. Min ◽  
Mark S. Cabatingan ◽  
Priscilla A. Schaffer

ABSTRACT Technical challenges associated with mutagenesis of the large oriL palindrome have hindered comparisons of the functional roles of the herpes simplex virus type 1 (HSV-1) origins of DNA replication, oriL and oriS, in viral replication and pathogenesis. To address this problem, we have developed a novel PCR-based strategy to introduce site-specific mutations into oriL and other large palindromes. Using this strategy, we generated three plasmids containing mutant forms of oriL, i.e., pDoriL-IL, pDoriL-IR, and pDoriL-ILR, containing point mutations in the left, right, and both copies, respectively, of the origin binding protein (OBP) binding site (site I) which eliminate OBP binding. In in vitro DNA replication assays, plasmids with mutations in only one arm of the palindrome supported origin-dependent DNA replication, whereas plasmids with symmetrical mutations in both arms of the palindrome were replication incompetent. An analysis of the cloned mutant plasmids used in replication assays revealed that a fraction of each plasmid mutated in only one arm of the palindrome had lost the site I mutation. In contrast, plasmids containing symmetrical mutations in both copies of site I retained both mutations. These observations demonstrate that the single site I mutations in pDoriL-IL and pDoriL-IR are unstable upon propagation in bacteria and suggest that functional forms of both the left and right copies of site I are required to initiate DNA replication at oriL. To examine the role of oriL and oriS site I in virus replication, we introduced the two site I mutations in pDoriL-ILR into HSV-1 DNA to yield the mutant virus DoriL-ILR and the same point mutations into the single site I sequence present in both copies of oriS to yield the mutant virus DoriS-I. In Vero cells and primary rat embryonic cortical neurons (PRN) infected with either mutant virus, viral DNA synthesis and viral replication were efficient, confirming that the two origins can substitute functionally for one another in vitro. Measurement of the levels of oriL and oriS flanking gene transcripts revealed a modest alteration in the kinetics of ICP8 transcript accumulation in DoriL-ILR-infected PRN, but not in Vero cells, implicating a cell-type-specific role for oriL in regulating ICP8 transcription.


2002 ◽  
Vol 76 (22) ◽  
pp. 11541-11550 ◽  
Author(s):  
Bruno Sainz ◽  
William P. Halford

ABSTRACT In vivo evidence suggests that T-cell-derived gamma interferon (IFN-γ) can directly inhibit the replication of herpes simplex virus type 1 (HSV-1). However, IFN-γ is a weak inhibitor of HSV-1 replication in vitro. We have found that IFN-γ synergizes with the innate IFNs (IFN-α and -β) to potently inhibit HSV-1 replication in vitro and in vivo. Treatment of Vero cells with either IFN-β or IFN-γ inhibits HSV-1 replication by <20-fold, whereas treatment with both IFN-β and IFN-γ inhibits HSV-1 replication by ∼1,000-fold. Treatment with IFN-β and IFN-γ does not prevent HSV-1 entry into Vero cells, and the inhibitory effect can be overcome by increasing the multiplicity of HSV-1 infection. The capacity of IFN-β and IFN-γ to synergistically inhibit HSV-1 replication is not virus strain specific and has been observed in three different cell types. For two of the three virus strains tested, IFN-β and IFN-γ inhibit HSV-1 replication with a potency that approaches that achieved by a high dose of acyclovir. Pretreatment of mouse eyes with IFN-β and IFN-γ reduces HSV-1 replication to nearly undetectable levels, prevents the development of disease, and reduces the latent HSV-1 genome load per trigeminal ganglion by ∼200-fold. Thus, simultaneous activation of IFN-α/β receptors and IFN-γ receptors appears to render cells highly resistant to the replication of HSV-1. Because IFN-α or IFN-β is produced by most cells as an innate response to virus infection, the results imply that IFN-γ secreted by T cells may provide a critical second signal that potently inhibits HSV-1 replication in vivo.


1985 ◽  
Vol 76 (2) ◽  
pp. 239-246 ◽  
Author(s):  
Sytske Welling-Wester ◽  
Bertha A. Huitema ◽  
Jan B. Wilterdink

2016 ◽  
Vol 17 (2) ◽  
pp. 1-8
Author(s):  
Simon Alem ◽  
Festus Tolo ◽  
Nicholas Adipo ◽  
Peter Mwitari ◽  
Ngetich Japheth ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document