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Herpes simplex virus latency in immunosuppressed mice
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Microbiologica
Volume 7, Issue 3, July 1984, Pages 219-227
Herpes simplex virus latency in immunosuppressed mice. (Article)
Rotula, A., Di Luca, D., Gerna, G., Manservigi, R., Tognon, M., Cassai, E.
Abstract
To determine the role of antibodies in establishing Herpes simplex virus (HSV) latency, immunosuppressed Swiss mice were experimentally infected in the right hind footpad with a HSV-1 x HSV-2 recombinant (C6D) with low virulence. Immunosuppression was induced by repeated intraperitoneal inoculations of Cyclophosphamide (CY) and the production of antibodies to C6D in immunosuppressed animals was monitored by Enzyme Linked Immunosorbent Assay (ELISA). Within 21 days after inoculation, C6D was able to establish a latent infection of lumbosacral spinal ganglia in both normal and CY-treated immunosuppressed animals. The data presented indicate that detectable production of antibodies is not necessary to induce HSV latency in spinal ganglia
An overview of letermovir: a cytomegalovirus prophylactic option
No full textIntroduction: Human cytomegalovirus (HCMV) or human herpesvirus 5 (HHV-5) is a β-herpesvirus that causes widespread infection in nearly all members of the human population worldwide. Its persistence in humans after primary infection in a latent phase as well as a partial non–protective immune response is the basis for repeated re-activation/re-infection episodes occurring both in immunocompetent and immunocompromised subjects. In the latter patient populations, which include hematopoietic stem cell transplant (HSCT) recipients, HCMV reactivation episodes may be particularly severe, leading to both systemic and end-organ diseases. Since the 90s, at least four antiviral drugs targeting the DNA polymerase complex have been developed for the prevention and treatment of HCMV infections in transplant recipients, used as first-line (ganciclovir and valganciclovir) and second-line therapy (foscarnet and cidofovir). However, due to their toxicity and drug-resistance induction, new drugs with different targets were needed. Areas covered: In 2017, a new drug named letermovir (LTV), which targets the HCMV DNA terminase complex, was licensed for prophylaxis of HCMV infections in HSCT recipients. This is the focus of this review. Expert opinion: LTV safety and efficacy are promising. However, long-term adverse events and the emergence of drug-resistant HCMV strains must be investigated in extended clinical trials prior to drawing final conclusions
Identification of a human cytomegalovirus mutant in the pp150 matrix phosphoprotein gene with a growth-defective phenotype
No full textFollowing amplification by PCR of a portion of the matrix phosphoprotein pp150 gene, electrophoretic analysis revealed the simultaneous presence of two viral variants of human cytomegalovirus in the blood of a heart transplant recipient. Repeated denaturation-annealing cycles during the amplification reaction led to the formation of heteroduplex molecules with altered electrophoretic mobility. Sequence analysis of the amplification products showed the presence of a viral variant carrying an in-frame three nucleotide deletion, which caused the absence of an aspartic acid in the corresponding protein. Attempts to plaque-purify the deletion mutant were unsuccessful, suggesting that the variant was growth-defective
Rapid quantitation of human cytomegalovirus DNA by PCR in blood of immunocompromised patients
No full textRestriction fragment length analysis and single strand conformation analysis in the study of the molecular epidemiology of human cytomegalovirus
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A point mutation in the thymidine kinase gene is responsible for acyclovir-resistance in herpes simplex virus type 2 sequential isolates
No full textA number of HSV-2 isolates, sequentially recovered from ulcerative ano-genital lesions of an AIDS patient during a prolonged treatment with acyclovir (ACV), have been studied at the molecular level. All of them were highly resistant to ACV (ACV-r) and shown to be virtually deficient in thymidine kinase (TK) activity. The ACV-r phenotype was demonstrated to be due to the production of truncated TK polypeptide. Structural alteration of this gene, as shown in one isolate, was caused by a chain-terminating mutation that originated from a cytidine deletion at position 520 of the TK open reading frame. This mutation generated a TGA stop codon 27 nucleotides downstream. An additional isolate was also recovered following ACV discontinuation and after a cycle of treatment with foscarnet. This isolate had lost the ACV-r trait and was characterized by a wild type TK sequence and by the production of a functional enzyme. Data presented confirm that a prolonged treatment with acyclovir can easily select ACV-r HSV-2 isolates carrying a TK- phenotype caused by a frameshift mutation. Although recovered from lesions tributary of different myelomers, these isolates may belong to the same strain that has undergone multiple cycles of reactivation and has possibly mutated during its axonal route to the skin
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