Jordan Richards
BIOB 425
Paper #1
Assembly of endocytic machinery around individual influenza viruses during viral entry
The purpose of this paper was to determine the entry method of influenza by tracking an individual influenza virus and endocytic structures in living cells. The main focus of entry was clathrin-mediated pathways and clathrin- and caveolin- independent pathways. These pathways were further researched to understand the development and use of clathrin-coated pits (CCP) and clathrin-coated vesicles (CCV). This experiment was done by using a series of methods that allowed for fluorescent labeling, immunofluorescence, and fluorescence imaging. The viruses were labeled with DiD which allowed for visualization in the experiments. ……. Florescence imaging was used to obtain multiple images of the DiD labeled viruses. This was accomplished by using a laser to excite the tags. Green and red dyes can be seen together or separately depending on the wavelength used during viewing. The images were analyzed by determining peaks.
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First, the internalization of the virus was determined. Three stages were identified for the internalization to occur. These stages are as follows: Stage I- actin dependent movement on the cell surface. Stage II- Unidirectional movement toward the nucleus by use of microtubules. At this stage the virus is inside the cell and headed toward the lysosome. Internalization was found to occur at about 190 seconds. Stage III- Bidirectional movement within the cell and is dependent on microtubules as well. It was determined through experimentation that microtubule movement only occurs once internalization of the virus has
This virus searches for a new vulnerable host in order to survive and carry the disease to the next victim. The critical aspect around the spread of a virus is how drastically the reproduction process occurs. Without being controlled, the contamination throughout any species causes the spread to take place in a toxic way, “On day one, there were two people. And then, four, and then, sixteen. In three months, it’s a billion.
However due to globalization, import and export viruses is more easily transmitted. Over the past century the global community especially Asian has been affected with new strains of the influenza virus. The changes in the virus can occur in two ways “antigenic drift” which are gradual changes in the virus over time. This change produces new strains that the antibody may not recognize. “Antigenic shift” On the other is a sudden change in the influenza virus which ‘’ results in a new influenza A subtype or a virus with a hemagglutinin or a hemagglutinin and neuraminidase combination that has emerged from an animal population,” as seen with H5N1 virus. This change leaves people defenseless against this new virus. (CDC, 2013) Currently there is no vaccine to combat all strains therefore “Planning and preparedness for implementing mitigation strategies during a pandemic requires participation by all levels o...
Then it enters into the host by exchanging its DNA or RNA. The virus then
Influenza, or the "flu," is an infection that is caused by the influenza virus. It is a virus that generally infects the olfactory organ, pharynx, and it can sometimes spread to the lungs (2007). Symptoms of influenza can be identified as acute fever, cough, chills, fatigue, body aching and, in young children, ear aches. Unlike the viruses that cause the common cold, the influenza virus can cause severe illnesses like pneumonia, especially in those who are very young or very old, or who have conditions such as cancer, heart disease, bronchial asthma and diabetes. Influenza can be spread by something as simple as an infected individual coughing or sneezing, through little droplets that go up to a meter (3 feet) and land on any nearby individuals
The virus is primarily spherical shaped and roughly 200nm in size, surrounded by a host-cell derived membrane. Its genome is minus-sense single-stranded RNA 16-18 kb in length. It contains matrix protein inside the envelope, hemagglutinin and neuraminidase, fusion protein, nucleocapsid protein, and L and P proteins to form the RNA polymerase. The host-cell receptors on the outside are hemagglutinin and neuraminidase. The virus is allowed to enter the cell when the hemagglutinin/ neuraminidase glycoproteins fuse with the sialic acid on the surface of the host cell, and the capsid enters the cytoplasm. The infected cells express the fusion protein from the virus, and this links the host cells together to create syncitia.
Loo, Yueh-Ming and Michael Gale, Jr. “Influenza: Fatal Immunity and the 1918 Virus.” Nature 445 (2007): 267-268. 23 July. 2008 .
In this book they talk about how the virus attaches itself to “host cells,” such as living human/animal cells, and from there it damages the all of the cells in the body by multiplication. Once the virus has taken over all of the living cells in one person or animal, it jumps to the next living cell it can find, causing an amplification of the virus. Once the virus cannot find another host cell, the virus “vanishes,” but it doesn’t go away. It is just waiting for the next victim to come along. This emphasizes the importance of the working with this virus in a biocontainment facility that is made especially for pathogenic viruses and bacteria like Ebola.
Philadelphia was overcrowded with people. At the time it was also common of its war experiences. People were out looking for jobs. Boy Scouts were on a lookout to find rooms for incoming families. And sometimes even Two, Three, or Four families would crowd in a single or two room apartment with kids. Teens shared beds and laborers did too. During winter of 1917-1918 the death rates had gone up according to the Health Department. They offered social services that were very poor. It was known as the “Blockley” which was an asylum, hospital, and poorhouse. There was Charitable activities ran by the Social Elite. Even schools were short in supplies and there were no high schools until 1934. All this overcrowded population caused an infectious disease. The city government did not take responsibility for this crisis. Neither did Dr. Wilmer Krusen who was the director of the Department of public health. He didn’t have no rush and he always believed that problems disappeared on their own.
At no time was a search for the cure for influenza more frantic than after the devastating effects of the pandemic of 1918. The pandemic killed somewhere between twenty and a hundred million people, making it twenty five times more deadly than the ordinary cough and sneeze flu. The symptoms of this flu were like something straight out of a horror movie: the victim’s facial complexion changed to a dark, brownish purple, the feet turned black, and they began to cough up blood. Eventually, death was caused, literally by drowning, when the victim’s lungs filled with their own blood. The first scientist to claim to solve the enigma of influenza was Dr. Friedrich Johann Pfeiffer. He isolated a bacterium he named Hemophilus influenzae from the respiratory tract of those who had the flu in the pandemic of 1890. He was believed to be correct in his discovery until the pandemic of 1918, when scientists searched the respiratory tracts of influenza victims and only sometimes found his bacterium. Robert E. Shope and his mentor Paul Lewis were the next to attempt to crack the code of influenza. They chose to study the disease in pigs, a controversial choice because many people believed that the swine influenza pigs were contracting was not the same as the human flu. The first experiment they ran was ba...
The swine influenza or swine flu is a respiratory disease in pigs that is caused by the type A influenza viruses. These viruses are referred to as swine flu viruses but scientifically the main virus is called the swine triple reassortant (tr) H1N1 influenza virus. When the viruses infect humans they are called variant viruses. This infection has been caused in humans mainly by the H1N1v virus in the United States. The H1N1 virus originates in animals due to improper conditions and the food they ingest. The virus stays in latency form, thus harmless to the respective animal. The longer the animals survive the more likely the virus is to develop and strengthen making it immune to vaccines. The virus reproduced through the lytic cycle. The virus injects its own nucleic acids into a host cell and then they form a circle in the center of the cell. Rather than copying its own nucleic acids, the cell will copy the viral acids. The copies of viral acids then organize themselves as viruses inside of the cell. The membrane will eventually split leaving the viruses free to infect other cells.
The “Aussie flu”, an Australian influenza virus, has made headlines on media worldwide. It is suggested that the Australian strain has spread to other countries, which has led to criticism of Australia’s Public Health policies. Although, is it possible to identify a strain’s source? If so, how did this “Aussie flu” become so harmful, could it have been prevented? The media is comparing this year’s flu outbreak to the 1968 Hong Kong flu, is it really the next flu pandemic? Influenza viruses are ever evolving and resisting to antibiotic treatment. This is a Global Health issue, particularly making an impact in Australia.
Viruses are important to discuss because they are analyzed in almost all microbiology classes. Viruses can be characterized as, “any of a group of submicroscopic entities consisting of a single nucleic acid chain surrounded by a protein coat and capable of replication only within the cells of living organisms” (Biology). Bacteriophage are more specific in a sense that they are “a virus that infects and replicates within a bacterium” not just any living organisms cells (Biology). These viruses can replicate in 2 different cycles: lytic cycle or the lysogenic cycle. If a virus takes enters the lytic cycle it will cause infection and destruction of the host cell. This is done when the virus first penetrates the cell membrane of the host cell.
The influenza virus is an RNA virus has an envelope that included members of the family Orthomyxoviridae. Its genome is a single negative strand segmented RNA. This virus consists of three types: A, B, and C. Influenza types A and B has eight segments of RNA, but the influenza virus type C only has 7 segments (Cheung and Poon, 2007). Influenza A virus is a virus that spread and infect many species of animals such as pigs, horses, cats, tigers, leopards, marine mammals and fowl and including humans. Type A viruses are divided into several subtypes were composed out of two (2) types of glycoproteins on the surface. These proteins are called hemagglutinin (HA) and Neuraminidase (NA) (Cheung and Poon, 2007).
The DENV envelope protein E, which is found on the virus surface, has a role as a mediating factor in the initial attachment of the virus to the host cell. Further, several cellular proteins and carbohydrate molecules that act as attachment factors interacting with the viral envelope protein E have been identified. These factors allow the virus population to concentrate on the cell surface thus increasing their chance of access to their target cellular receptor(s). Some of these known molecules that interact with the vi...
In 1918-19 approximately 50 million deaths were a detriment of the Spanish H1N1 virus pandemic; a respiratory virus. According to the World Health Organization, the second Influenza A H1N1 pandemic in 2009 spread to more than 200 countries causing more than 18 000 deaths. Before the World Health Organization had announced the official end of the pandemic in August 2010, in July 2009 the World Health Organization sent out a phase 6 warning that H1N1 could soon be a global pandemic. It is important to recognize that the 2 different outbreaks had different A/H1N1strains effecting the world population; this suggests A/H1N1has a high ability for mutation, severely complicating the human body’s natural immune mechanism of antigenic drift. (Qi-Shi Du et al., 2010)