question archive 1) How and what causes spongiform encephalopathy? 2

1) How and what causes spongiform encephalopathy? 2

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1) How and what causes spongiform encephalopathy?

2. Give major differences between prokaryotic and eukaryotic transcription and translation.

3. Explain in detail the process of temperate phage infection. Name the bacteriophage that was used as a model to study this process.

4.List five steps of infections cycle of the animal virus. Explain in detail the

 

replication of RNA and Reverse-transcribing viruses

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Answer:

1. How and what causes spongiform encephalopathy? 

Transmissible spongiform encephalopathies are caused by prions, infectious proteins that appear to replicate by converting a normal cellular protein into copies of the prion. 

Causes

Viral hypothesis: This hypothesis postulates that an as of yet undiscovered infectious viral agent is the cause of the disease. Evidence for this hypothesis is as follows:

  • Incubation time is comparable to a lentivirus
  • Strain variation of different isolates of PrPSc
  • An increasing titer of PrPSc as the disease progresses suggests a replicating agent.

Multi-component hypothesis: While not containing a nucleic acid genome, prions may be composed of more than just a protein. Purified PrPC appears unable to convert to the infectious PrPSc form, unless other components are added, such as RNA and lipids. These other components, termed cofactors, may form part of the infectious prion, or they may serve as catalysts for the replication of a protein-only prion.

Genetics: Mutations in the PRNP gene cause prion disease. Familial forms of prion disease are caused by inherited mutations in the PRNP gene. Only a small percentage of all cases of prion disease run in families, however. Most cases of prion disease are sporadic, which means they occur in people without any known risk factors or gene mutations. In rare circumstances, prion diseases also can be transmitted by exposure to prion-contaminated tissues or other biological materials obtained from individuals with prion disease.

 

2. Give major differences between prokaryotic and eukaryotic transcription and translation.

  • In eukaryotes, transcription, and translation take place in different cellular compartments: transcription takes place in the membrane-bounded nucleus, whereas translation takes place outside the nucleus in the cytoplasm. In prokaryotes, the two processes are closely coupled. 
  • eukaryotic and prokaryotic translation is that eukaryotic translation and transcription is an asynchronous process whereas prokaryotic translation and transcription is a synchronous process.


3. Explain in detail the process of temperate phage infection. Name the bacteriophage that was used as a model to study this process.

Temperate phages are bacteriophages that can choose between the lytic and the lysogenic pathways of development. The lytic pathway is similar to that of virulent phages. In the lysogenic pathway, the virus remains dormant until induction. Temperate bacteriophages start their life cycle when they adsorb to a permissive host. After injecting their genome into the host cell, they produce a set of early proteins and a few copies of their genome. At this stage, a decision "lysis versus lysogeny" is made. Usually, in poor growing conditions of the host cell the phage chooses the lysogenic pathway because the number of progeny it can produce in such cell is usually low. When lysogeny is chosen, the phage integrates its genetic material with the host cell. It may be done by physical incorporation of the phage genome into the host genome, or the prophage may be integrated as a stably maintained plasmid. When a prophage is induced, it starts to produce viral proteins and copies of the viral genome using bacterial resources and biosynthetic apparatus.

 

Lambda phage is used to study the process.

 

4. List five steps of the infection cycle of the animal virus. 

  • Attachment: The attachment refers to the first encounter of virus particles with host cells, which involves two kinds of host proteins on the plasma membrane: (1) attachment factors and (2) viral receptors. The attachment factor on the cell surface recruits and holds the virus particles, thereby facilitating the interaction of the viral particle with the entry receptor. 
  • Penetration: Following the attachment of the virus particle to the target cells, the next step is penetration into the cytoplasm. The mechanism for the penetration differs, whether enveloped or not. For enveloped viruses, one of the following two mechanisms is used: direct fusion and receptor-mediated endocytosis. For nonenveloped naked viruses, receptor-mediated endocytosis is used for penetration.
  • Capsid Assembly: The capsid assembly follows as the viral genome as well as the viral proteins abundantly accumulate. The capsid assembly can be divided into two processes: capsid assembly and genome packaging. Depending on viruses, these two processes can occur sequentially or simultaneously in a coupled manner.
  • Release: For naked viruses, the virus particles are released via cell lysis of the infected cells. Thus, no specific exit mechanism is necessary, because the cell membrane that traps the assembled virus particles is dismantled.
  • Maturation: The last step of the virus particle assembly is "maturation," a process that occurs extracellularly the following release. 

Explain in detail the replication of RNA and Reverse-transcribing viruses

RNA viruses replicate their genomes using virally encoded RNA-dependent RNA polymerase (RdRp). The RNA genome is the template for synthesis of additional RNA strands. During replication of RNA viruses, there are at least three types of RNA that must be synthesized: the genome, a copy of the genome (copy genome), and mRNAs. Some RNA viruses also synthesize copies of subgenomic mRNAs. RdRp is the key player for all of these processes. RdRps of all RNA viruses probably arose from a common ancestor. The RdRp and other proteins required for viral genome synthesis are often called the replicase complex. 

Source: 

Mahon's Medical Microbiology

Ryu W. S. (2017). Virus Life Cycle. Molecular Virology of Human Pathogenic Viruses, 31-45. https://doi.org/10.1016/B978-0-12-800838-6.00003-5