Sequence analysis of the herpes simplex virus type 1 strain 17 variants 1704, 1705 and 1706 with respect to their origin and effect on the latency-associated transcript sequence.

نویسندگان

  • F Junejo
  • A R MacLean
  • S M Brown
چکیده

The precise endpoints of the deletions/insertions in three variants (1704, 1705 and 1706) of herpes simplex virus type 1 (HSV-1) strain 17 have been determined by dideoxynucleotide sequence analysis. The analysis was undertaken to discover whether the three variants had arisen from the same initial event and the extent of the deletions with respect to the latency-associated transcripts (LATs) and the proposed LAT promoter region. It is not possible from the deletion boundaries to determine unequivocally whether the three variants had arisen from the same recombination event although 1706 could be descended from 1705 by illegitimate recombination. The results demonstrate that spontaneous deletions can occur at random within RL, the extent of the deletions in UL is constrained by the essential nature of UL genes in vitro but is otherwise arbitrary and deletions in 1704 completely remove both copies of the LAT promoter region and in IRL extend into the 5' end of the LAT sequence.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Herpes Simplex Virus Type 1 Latency-Associated Transcript Reduces Human Neuroblastoma Cell Proliferation

Background and Aims: The latency-associated transcript (LAT) transcribed by latent Herpes Simplex Virus type-1 in neuron cells are able to influence their host cell pathways. While the most of previous studies were focused on anti-apoptotic effects of LAT, our investigation is making an effort to explore LAT potency on cell cycle pathway in neuroblastoma cell lines. Methods: The evaluation of L...

متن کامل

Replication Characteristics of Herpes Simplex Virus Type-1 (HSV-1) Recombinants in 3 Types of Tissue Cultures

A complication in the analysis of the role of ICP34.5 gene in the herpes simplex virus type-1 (HSV-1) lifecycle is the presence of overlapping antisense gene, open reading frame P (ORF P), which is also deleted in HSV-1 ICP34.5 negative mutants. A HSV-1 wild type strain (17+) ICP34.5/ORF P deletion mutant (1716) is totally avirulent in animal models and impaired in a number of in vitro function...

متن کامل

PCR detection of thymidine kinase gen of latent herpes simplex Virus type 1 in mice trigeminal ganglia

  Herpes simplex virus type 1 establishes a latent infection in the peripheral nervous system following primary infection. During latent infection, virus genome exhibit limited transcription, with the HSV LATs consistently detected in latency infected ganaglia. Following ocular infection viral latency develops in the trigeminal ganglia. In this study PCR has been used for detection of HSV-1 nuc...

متن کامل

S1 gene sequence analysis of infectious bronchitis virus vaccinal strains (H120 & H52) and their embryo-passaged derivatives

Avian infectious bronchitis is an acute and highly contagious disease that mainly causes respiratory symptoms in poultry. A number of serotypes and variants of the viral agent with poor cross-protection are the major problem to achieve desired immunity from vaccination. The S1 subunit of S glycoprotein (spike) is the major determinant of IBV so that a minor change in amino acid sequence of this...

متن کامل

Comparative Molecular PCR-RFLP Study of Native Herpes Simplex Virus Type 1 (HSV-1) with KOS Strain

Background: Recent research on several DNA fragments covering open reading frames (ORF) 1-37 shows a new genetic marker in ORF 6 which is specific for differentiating wild-type varicella-zoster virus (VZV) strains from Oka varicella vaccine strain. On the other hand, herpes simplex virus (HSV) genome analysis by restriction enzymes is used to differentiate types one and two of the virus and eve...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • The Journal of general virology

دوره 72 ( Pt 9)  شماره 

صفحات  -

تاریخ انتشار 1991