Question

Review the items below and then read relevant sections of Ch. 6, pg. 123-129, Ch. 27. pgs. 607-608 and Ch. 38 pgs. 828-829, 856-857 to help prepare responses for submission on BB. 1. Describe what prions are and explain how they are thought to replicate. Identify and describe a disease caused by prions. 2. Compare and contrast the 4 different types of viral infections that can occur in animals (see Figure 6.17). Address both the impact on the individual infected host cell and the whole organism. 3. Some cancers are caused by viruses. Explain one mechanism by which these viruses (oncoviruses) trigger cancerous transformation of cells. Your answer should address what happens to an affected cell at the level of its DNA and clearly indicate the role of the virus in these changes. 4. Keeping in mind the general steps of viral replication we discussed in Ch. 6, describe what specifically happens at each step when the Herpes Simplex Virus Type 1 replicates. 5. Explain why cold sores reoccur throughout the lifetime of an HSV-1-infected individual. Explain the relationship between chickenpox and shingles.

Answer 1

HI THERE,

ALTHOUGH YOU DIDNT PROVIDED THE FIGURE, STILL, I WILL TRY TO ANSWER

ANSWER 1

Prions are a small proteinaceous infectious disease-causing agent that is believed to be the smallest infectious particle. A prion is neither bacterial nor fungal nor viral and contains no genetic material. Prions have been held responsible for a number of the degenerative brain are unprecedented infectious pathogens that cause a group of invariably fatal neurodegenerative diseases by an entirely novel mechanism.

Prion diseases may present as genetic, infectious, or sporadic disorders, all of which involve modification of the prion protein (PrP). Bovine spongiform encephalopathy (BSE), scrapie of sheep, and Creutzfeldt-Jakob disease (CJD) of humans are among the most notable prion diseases. Prions are transmissible particles that are devoid of nucleic acid and seem to be composed exclusively of a modified protein (PrPSc).

HOW PRIONS REPLICATE?

There are two models predicting replication in prions.

1. Heterodimer model

2. Fibril model

HETRODIMER MODEL assumed that a single PrPSc molecule(an infectious isoform of PrP, ) binds to a single PrPC molecule( a normal protein found on the membranes of cells.) and catalyzes its conversion into PrPSc. The two PrPSc molecules then come apart and can go on to convert more PrPC. However, a model of prion replication must explain how prions propagate, and why their spontaneous appearance is so rare. Manfred Eigen showed that the heterodimer model requires PrPSc to be an extraordinarily effective catalyst, increasing the rate of the conversion reaction by a factor of around 1015. This problem does not arise if PrPSc exists only in aggregated forms such as amyloid, where cooperativity may act as a barrier to spontaneous conversion.

2. FIBRIL MODEL  assumes that PrPSc exists only as fibrils, and that fibril ends bind PrPC and converts it into PrPSc. then the number of prions would increase linearly, forming ever longer fibrils. But the exponential growth of both PrPSc and of the number of infectious particles is observed during prion disease.

DISEASE CAUSED BY PRIONS

CREUTZFELDT JAKOB DISEASE(CJD)  is a fatal degenerative brain disorder. Early symptoms include memory problems, behavioral changes, poor coordination, and visual disturbances. Later symptoms include dementia, involuntary movements, blindness, weakness, and coma.

CJD is caused by a protein known as a prion. Infectious prions are misfolded proteins that can cause normally folded proteins to become misfolded. About 85% occur spontaneously, while about 7.5% of cases are inherited from a person's parents in an autosomal dominant manner. Exposure to the brain or spinal tissue from an infected person may also result in the spread. There is no evidence that it can spread between people via normal contact or blood transfusions. Diagnosis involves ruling out other potential causes. An electroencephalogram, spinal tap, or magnetic resonance imaging may support the diagnosis.

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ANSWER 2.

VIRAL INFECTIONS IN ANIMALS

VIRAL HEPATITIS viral hepatitis, an infection caused by a group of viruses that primarily affect the liver. Important forms of hepatitis to be discussed include hepatitis A (HAV), hepatitis B (HBV), hepatitis C (HCV). Hepatitis A is usually transmitted by the fecal-oral route. Infectious outbreaks occur where there is exposure to infected water or food. Hepatitis B virus transmission occurs via parenteral routes with transmission through contact with infected blood, through sexual transmission, and from mother to child in the perinatal period. Hepatitis c virus is responsible for the majority of cases of what was previously called non-A, non-B viral hepatitis. Routes of transmission are similar to those for hepatitis B although risk factors differ.

The main clinical features of the three types of viral hepatitis are similar with the most common features being fatigue, abdominal discomfort, jaundice (yellowing of the skin and whites of the eyes), and loss of appetite. Hepatitis A does not develop a chronic state although about 15 percent of patients experience a prolonged or relapsing course. Patients may have intermittent diarrhea and nausea. Hepatitis B infections present with similar symptoms usually several weeks following infection. The findings are initially similar to those described for HAV, including a rare patient with the fulminant disease who may die acutely from the infection.

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ANSWER 3.

VIRUSES CAUSING CANCER

When viruses cause an infection, they spread their DNA, affecting healthy cells’ genetic makeup and potentially causing them to turn into cancer. HPV infections, for instance, cause the virus’ DNA to combine with the host’s DNA, disrupting the normal function of cells. Other viruses, such as human immunodeficiency virus (HIV) and hepatitis C virus (HCV), may increase a person’s risk of developing cancer by affecting the body’s immune system. In most cases, specific viruses only affect specific cells in the body, such as common cold viruses that impact the lining of the nose and throat. That’s why certain viruses are only linked with certain kinds of cancer.

COMMON VIRUSES LINKED TO CANCER

1. The Epstein-Barr virus (EBV), which is a type of herpes virus most commonly associated with causing infectious mononucleosis, or “mono.” EBV infections increase the risk of nasopharyngeal cancer, some types of fast-growing lymphomas and some stomach cancers. Like HPV, EBV infections are common, but EBV-related cancer is not.

2. Hepatitis B virus (HBV) and HCV, which cause viral hepatitis, a kind of liver infection. HBV- and HCV-induced chronic liver infections are rare, but when they occur, they raise the risk of liver cancer. Less than half of liver cancers in the United States are linked to HBV or HCV infection.

3. HIV, which causes acquired immune deficiency syndrome (AIDS). HIV increases the risk for several types of cancer, including Kaposi sarcoma, cervical cancer, non-Hodgkin lymphoma, anal cancer, and lung cancer.

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HPV oncogenesis Host genome alterations Normal hrHPV CIN1 CIN2/3 Invasive Cancer • Surgery • Radiation • Chemotherapy • Advaxis, GN-00101 vaccines • Anti PD-1 antibodies • RNR, PARP inhibitors LEEP; Cryotherapy, Laser Therapy, Conization to prevent further progression

ANSWER 4.

HSV REPLICATION

herpesviruses follow these pathways

(1) HSV virion attaches to host cells with the envelope glycoprotein (gC) onto heparan sulfate moieties of cellular proteoglycans. Viral gD is believed to bind to a secondary cellular receptor.

(2) The viral envelope fuses to the plasma membrane in a pH-independent fashion such that the nucleocapsid enters the cytoplasm. gB, gD, and gH are instrumental glycoproteins for this phenomenon.

(3) The capsid travels along the cytoskeleton to a nuclear pore where the viral DNA is released. The linear genome enters the nucleus and circularizes.

(4) Once in the nucleus, the viral DNA is transcribed into mRNA by cellular RNA polymerase II. In herpesviruses, viral gene expression is tightly regulated and divided into 3 kinetic classes of expression.
* A tegument protein associates with 2 cellular proteins, and the complex transactivates transcription of HSV's five immediate-early (IE or alpha) genes. IE genes generally encode regulatory proteins.
* An IE protein initiates transcription of the early (E or beta) genes. These gene products are enzymes needed to increase the pool of nucleotides and for viral replication.
* Lastly, late (L or gamma) genes are activated for the production of viral structural proteins.

(5) After transcription in the nucleus, all mRNA transcripts are translated into protein in the cytoplasm. Subsequently, the proteins can go to the nucleus, stay in the cytoplasm, or become a part of the membrane bilayer.

(6) Capsid proteins assemble in the nucleus to form empty capsids.

(7) Full-length viral DNA is packaged to form nucleocapsids.

(8) The nucleocapsids associate with segments of the nuclear membrane where tegument and glycosylated envelope proteins have bound. This association triggers envelopment by budding through the nuclear membrane.

(9) Enveloped virions accumulate in the endoplasmic reticulum (ER).

(10) Mature virions are released by exocytosis.

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ANSWER 5.

PART 1.

Why cold sores reoccur through the lifetime of HSV 1 INFECTED INDIVIDUAL?

Once a person contracts the herpes simplex virus (HSV-1), it usually causes an initial outbreak of cold sores.

Then, the virus remains in the person’s body for the rest of their life, causing new cold sores to form randomly when it reactivates.

If a person keeps getting cold sores, there may be an underlying cause. Many factors can trigger reactivation and subsequent cold sore outbreaks, including:

• hormonal changes, such as those associated with pregnancy or menopause
• another viral infection or illness
• exposure to sunlight, wind, or cold
• stress
• fatigue
• immune system changes

The virus that causes cold sores is extremely contagious, even when a person does not have cold sores.

A person can contract or spread HSV-1 through sharing utensils, food, and beverages. Kissing and engaging in oral sex can also spread the virus. Oral sex may also spread HSV-2, which usually causes genital herpes.

PART 2.

RELATIONSHIP BETWEEN CHICKENPOX AND SHINGLES

The same virus that causes chickenpox also causes shingles!

Although shingles and chickenpox are caused by the same virus, they are not the same illness. Chickenpox is usually a milder illness that affects children. Shingles result from a reactivation of the virus long after the chickenpox illness has disappeared. The chickenpox virus stays in the body even after recovery. Later in life, the virus can reactivate and cause shingles. If you have shingles, you can spread the varicella virus to people who have never had chickenpox or never received the chickenpox vaccine. These people will develop chickenpox, not shingles. It takes from 10 to 21 days after exposure to chickenpox or shingles for someone to develop chickenpox.

CHICKENPOX(VARICELLA)

• Initial symptoms include sudden onset of fever, headache, and feeling tired.

• An itchy blister-like rash, usually starting on the face, chest or back, follows 1-2 days later.

• The rash then spreads to the rest of the body, and new blisters continue to appear for about 3-4 days.

• Generally, within 1 week, the blisters dry out and scabs form and fall off.

Chickenpox is very contagious. The virus can spread by breathing in the viral particles that come from the blisters. It can also be spread by direct contact with the fluid of skin lesions. A person with chickenpox can spread the disease from 1 to 2 days before they get the rash until all their chickenpox blisters have formed scabs

There are two vaccine options:

• Two doses of the varicella vaccine.

• A combination vaccine called MMRV (measles, mumps, rubella, and varicella)

SHINGLES(HERPES ZOSTER)

• The first sign is often a tingling feeling on the skin, itchiness, or stabbing pain.

• After several days, a rash appears, beginning as a band or patch of raised dots on the side of the trunk or face or other areas of the body.

• It then develops into small, fluid-filled blisters that begin to dry out and crust over within a few days.

• When the rash is at its peak, symptoms can range from mild itching to extreme and intense pain.

• The rash and pain usually disappear within 3-5 weeks.

Shingles cannot be passed from one person to another. Someone with an infectious shingles rash can spread chickenpox if the other person has never had chickenpox. However, someone with shingles will not cause another person to develop shingles.

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