Lassa Virus

When we hear the word virus, we usually think of something that makes us sick. A virus is an ultramicroscopic infectious organism that, having no independent metabolic activity, can replicate only within a cell of another host organism. A virus consists of a core of nucleic acid, either RNA or DNA, surrounded by a coating of antigenic protein and sometimes a lipid layer surrounds it as well. The viral genome provides the genetic code for replication, and the host cell provides the necessary energy and raw materials. To fight viruses, we use vaccines. While some may infect a broad range, other viruses can only infect certain kinds of cells. Vaccines are made of inactive, dead or weakened virus cells or protein antigens that can no longer infect

Hand, foot, and mouth are parts of human body have the highest change to get contagious infection. There are many viruses but Enterovirus groups, (most common is the coxsackie virus) is the main factor. These viruses can spread through direct contact from person to person especially with those have bad habits such as: unusually washed hands or surfaces contaminated with feces. An infected person’s saliva, stool, or respiratory secretions can transmit the infection.

Viruses are microscopic particles that invade and take over both eukaryotic and prokaryotic cells. They consist of two structures, which are the nucleic acid and capsid. The nucleic acid contains all genetic material in the form of DNA or RNA, and is enclosed in the capsid, which is the protein coating that helps the virus attach to and penetrate the host cell. In some cases, certain viruses have a membrane surrounding the capsid, called an envelope. This structure allows viruses to become more stealthy and protected. There are two cycles in which a virus can go into: lytic and lysogenic. The lytic cycle consists of the virus attaching to a cell, injecting its DNA, and creating more viruses, which proceed to destroy the host. On the other hand, the lysogenic cycle includes the virus attaching to the cell, injecting its DNA, which combines with the cell’s DNA in order for it to become provirus. Then, the provirus DNA may eventually switch to the lytic cycle and destroy the host.

Measles is virus with a single-stranded RNA and two membranes: a fusion protein that infuses into the host cell membrane and the hemagglutinin protein that absorbs the virus into the cells. The primary site for invasion is in the epithelium of the nares. Measles is highly contagious and very infectious because it is easily transmitted when an infected person coughs or sneezes. The virus can stay in the air or on surfaces for up to two hours and infect many people who inhale the infectious agent or touch a surface, then be introduced to a new host through touch to

RSV belongs to the paramyxovirus family of viruses. The virion encompasses a helical nucleocapsid packaged in a lipoprotein envelope attained from the host cell plasma membrane during budding. The external surface of the envelope contains a periphery of surface spikes.

The virus fuses with the cell’s plasma membrane. The capsid proteins are removed, releasing the viral proteins and RNA. Reverse transcriptase catalyzes the synthesis of a DNA strand complementary to the viral RNA. Reverse transcriptase catalyzes the synthesis of a second DNA strand complementary to the first. The double-stranded DNA is incorporated as a provirus into the cell’s DNA. Proviral genes are transcribed into RNA molecules, which serve as genomes for the next viral generation and as mRNAs for translation into viral proteins. The viral proteins include capsid proteins and reverse transcriptase (made in the cytosol) and envelope glycoproteins (made in the ER). Vesicles transport the glycoproteins from the ER to the cell’s plasma membrane. Capsids are assembled around viral genomes and reverse transcriptase molecules. New viruses bud off from the host cell.

Nipah virus, Arena Virus and Francisella tularensis are bioterrorism agents. They work in various ways to harm the host. Francisella tularenis is considered a Tier 1 bioterrorism agent and Nipah virus is an overlap select agent that affects humans and agriculture both. They have been harmful in the past. Though, Nipah virus is a newer virus than the other two. This review will focus on their emergence, pathogenicity and symptoms of the diseases they cause.

Smallpox is a highly contagious infectious disease. The type of microbe for smallpox is the Variola virus. Smallpox is caused by either the Variola major or the Variola Minor. This virus is spread by direct contact. The disease was likely to be in human populations about 10,000 BC. An epidemic broke out in 1519 with the Aztecs and the Conquistadors in Tenochtitlan Mexico. The epidemic killed a total of twenty five percent of the Aztecs population leaving it easy for Cortes and the conquistadors to take over the desired

Smallpox is caused by the variola virus an extremely contagious disease. That can be spread through any type of contact with the virus. The virus is a member of the genus Orthopoxvirus, in the Poxviridae family. Smallpox has been considered eradicated in the United States since 1972. Virologists have speculated that it evolved from an African rodent poxvirus 10 millennia ago. The name is derived from the Latin word for "spotted" and refers to the raised bumps on the face and body of the patient. (Medscape.com) Smallpox has been to blame for the extinction and almost extinction of many cultures. The disease has been used as biological warfare since the beginning or war. At times,

RSV is caused by TLR3 activation. It initiates infections by binding to a cellular receptor and then the viral envelope fuses with the plasma membrane. The virus attaches the cell through the main protein, the G protein and fuses with the plasma membrane of the host cell through the F protein. After penetration, the nucleocapsid of the virus is released into the cytoplasm where replication occurs (3). The viral RNA is like a template for mRNA (3). The mRNA’s job is to translate the viral proteins and complementary RNA serves as a template for virion RNA

Hendra virus (originally called "Equine morbillivirus" was discovered in September 1994 when it caused the deaths of thirteen horses, and a trainer at a training complex in Hendra, a suburb of Brisbane in Queensland, Australia.[12]

The protective capsid helps the virus escape detection and destruction during the invasion of the host. When the virus reaches the target cell, biochemical reactions between the capsid and cell wall allow the virus to latch on and inject its genome into the cell’s interior. Once inside, the viral genetic material insinuates itself into the host’s DNA or RNA. In an efficient feat of natural bioengineering, the host cell’s genetic machinery now does the rest of the work for the virus. The cell, which had already been making copies of its own genome, now also replicates that of the virus. Coded within the viral material is the blueprint for making more copies of the viral genome. Further instructions command the production of capsids and directions for assembly of new viruses. After the host cell becomes engorged with viruses, it explodes, sending the new

The HIV-1 virion is approximately 120 nm in diameter, roughly spherical, and is composed of two copies of a single stranded positive sense RNA enclosed by a capsid (24). The HIV-1 genome is less than 10 kb and encodes for more than nine different gene products. It encodes for 3 major structural protein genes: gag (group-specific antigen), pol (DNA polymerase), and env (Envelope), which code for major structural proteins and essential enzymes. Gag generates the mature Gag protein matrix (MA or p17), capsid (CA or p24), nucleocapsid (NC or p7), and p6, which encompass proteins for the basic infrastructure of the virus such as the inner core of the viral particle (25). Pol encodes for reverse transcriptase (RT), which enables the virus to reproduce, integrase (IN), which is necessary to integrate the viral double stranded DNA into the host genome, RNAse H, and HIV protease, which are all encapsulated in the core of the inner particle formed by the viral capsid protein p24 (25). Env encodes for glycoproteins of the outer membrane such as outer gp120 (which enables the virus to attach and fuse to cells of the host), and transmembrane gp41 that anchors the glycoprotein complex to the surface of the virion (25). Between the core and the envelope is the HIV matrix proteins which are composed of the viral protein p17 (23). HIV-1 also encodes for proteins with important regulatory elements (tat (Trans-Activator of Transcription) and rev

The similarity between the poliovirus and already solved plant virus’s led to a better understanding of how the poliovirus can regenerate within a host. Although the virus was similar to other plant viruses. The poliovirus was covered with more elaborate loops that are the site of monoclonal antibody escape mutations (Hogle, Chow and 229: 1358-1365Filman, Science). Individual proteins of the virus particle are produced by proteolytic cleavages from a larger precursor, yet the amino and carboxy-termini produced by proteolysis are very distinct. By noting this, Hogle and his team were able to conclude that proteolysis was not just making a lot of proteins from one gene, it is also controlling the timing of assembly (Hogle, Chow and Filman, Science 229: 1358-1365).

Through Crystallographic Analysis, researchers were able to determine the structure of the viral NSP3 protein. The NSP3 protein is