Research papers on virus reproduction

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Research papers on virus reproduction

Retrovirus Replication Research Summary Stephen Goff is interested in the replication of two groups of retroviruses—the murine leukemia viruses and the human immunodeficiency viruses— and in the cellular gene products that interact with them.

His studies have defined the functions of many viral gene products, characterized host proteins that are exploited by the viruses, and identified new restriction factors that act to block virus replication. The retroviruses, a large family of RNA viruses found in all eukaryotes, include important pathogens such as the human immunodeficiency viruses HIVs.

Structural Biology for Virus Research

These viruses have an Research papers on virus reproduction lifestyle: As a direct result of the integration of the viral DNA into the host genome, retroviruses can cause an impressive variety of effects in an infected host. The viruses persist in the genome for the lifetime of an infected cell and an infected individual; they can even be transmitted to offspring in the germline as integrated DNA.

Many cause leukemias and other malignancies by inappropriately activating genes near the site of viral DNA insertion. They can also acquire host genes and carry them into newly infected individuals, causing a range of distinctive and aggressive tumors.

References

These properties make the retroviruses formidable pathogens. Blocking their replication will require a deep understanding of the functions of each of the viral proteins.

Transcriptional regulatory machinery involved in silencing retroviral DNAs in embryonic stem cells. Schematic representation of the host protein components of the transcriptional silencing complex bound to the Long Terminal Repeat LTR sequences of the Moloney murine leukemia virus DNA. Key players identified in the Goff lab are in color.

TRIM28 acts as a scaffold to recruit an array of proteins that mediate modifications to histones and chromatin to effectively shut off transcription of the viral genome.

HIV-1 Induces formation of stable microtubules in human cells. Microglial cell line CHME3 was mock infected or HIV-1 infected for 2 or 6 hours as indicated, and the cells were fixed and stained with antibodies specific for conventional "tyrosinated" microtubules Tyr-MTs; top row or "stable" acetylated AC-MTs; middle row.

HIV-1 infection leads to rapid induction of stable microtubules. Cell Host Microbe Horizontal transmission of a clonal cancer cell line in the soft-shell clam. Clam leukemia is transmitted horizontally between animals as contagious cancer cell clone red.

Michael Metzger Figure 4: Virus rapidly induces the formation of stable microtubules that promote efficient infection. Josef Sabo Early Events of Retrovirus Infection We are using a combination of biochemical and genetic methods to analyze the steps that occur early in infection.

We have isolated mutant cell lines that are resistant to retroviral infection by both the murine leukemia viruses MuLVs and HIVs, and we are using DNA-mediated transfection and DNA microarrays to identify and characterize the host genes involved in these steps.

Overexpression or underexpression of several host proteins such as IQGAP, moesin, and FEZ1, which are regulators of the cytoskeleton can profoundly block retroviral infection.

Some of these cell lines exhibit abnormalities in cytoskeletal structures and intracellular trafficking of surface receptors that correlate with their virus resistance.

Many genes controlling the formation of a specialized subset of microtubules—the so-called "stable" microtubules— have large effects on virus infection.

We have recently found that HIV-1 induces the formation of stable microtubules soon after entry into the cell to promote its movement toward the nucleus. Late Stages of Infection Our laboratory is also interested in the processes of viral gene expression and the assembly of virion particles, and many efforts have been directed toward identifying host genes involved in these stages of virus replication.

We have isolated dominant-acting mutant versions of several nuclear host proteins that block HIV-1 RNA formation and processing, identified components of transcriptional silencing complexes that block MuLV transcription in embryonic stem ES cells, and characterized a highly structured RNA suppressor of translational termination a so-called pseudoknot that is required for synthesis of the retroviral Pol gene products.

We have screened large mammalian cDNA expression libraries for genes that can block virus replication and have identified ZAP, a novel zinc finger protein with potent antiviral activity. Analysis of infected cells shows that overexpression of ZAP causes a profound and specific reduction in the levels of viral mRNA in the cytoplasm, without affecting levels in the nucleus.

ZAP exhibits potent activity against several other RNA viruses, including alphaviruses such as Sindbis virus, suggesting that it may represent part of an innate antiviral immune response. In a chronically infected cell, several viral proteins are brought together under the plasma membrane to form spherical particles that bud outward and are released from the cell surface.

The major player in assembly is the viral Gag protein, often called "the particle-making machine.

Research papers on virus reproduction

These studies included analysis of Gag-Gag interactions, the dimerization of the subunits of reverse transcriptase RTand the trimerization of the transmembrane subunits of the envelope protein.

We have also identified several novel host proteins that bind to the Moloney MuLV Gag precursor including the endophilins, likely involved in inducing membrane curvatureto RT, to the viral integrase enzyme, and to the envelope protein. Some of these proteins are incorporated into virion particles, and dominant-negative forms of several others can act to suppress virion assembly and release.

Epigenetic Silencing of Retroviral Transcription in Embryonic Stem Cells Retrovirus replication is strongly restricted in mouse ES and embryonic carcinoma cells at the level of transcription. Silencing of retroviruses in these pluripotent cells is likely to have evolved to protect the embryo not only from infection but also from the reactivation of endogenous retroviruses and retrotransposons that could cause damaging mutations in the germline and early progenitor cells.Research indicates that the virus utilises a lipid-dependent, non-clathrin and dynamin-independent endocytic pathway of entry.

Macropinocytosis is the most likely mechanism employed by the Ebola virus . Virology News.

Read current research on the virus structure, specific viruses (H5N1 flu, West Nile virus, HIV and more) and responses. Let's look at what happens when a virus attacks our cells.

Most viruses reproduce through a process called lytic vetconnexx.com lytic infection, a virus enters the host cell, makes a copy of itself, and causes the cell to burst, or vetconnexx.com the video Virus Lytic Cycle, a bateriophage, which is a virus that infects and replicates within a bacterium, attaches .

Research Papers on Computer Viruses Computer Viruses is a program file capable of reproducing its own special code and attaching that code to other files without the knowledge of the user.

Virus Research - Journal - Elsevier

Research papers on computer viruses change frequently. Genetic fusion of peste des petits ruminants virus haemagglutinin and fusion protein domains to the amino terminal subunit of glycoprotein B of bovine herpesvirus 1 interferes with transport and function of gB for BHV-1 infectious replication.

The tail directly comes in contact with bacte­rial cell, drills a hole in the wall and injects the phage DNA into the cell. In lysogenic cycle, the phage DNA does not take over the control of cellular machin­ery of the host.

Types of Reproductive Cycle in Virus