Monthly Archives: January 2009

Interesting news

December 30, 2003

Prion proteins may store memories

Study hints at vital job for two-faced proteins.

Mystery proteins called prions, which can flip between two different shapes, might help in laying down memories, according to US researchers. The finding hints at an entirely new set of roles for the proteins.

Prions are unusual in the protein world: when they adopt one of their guises, they can reproduce, converting other identical proteins into copies of themselves. Often such replicating prions are harmful – they clog up the brains of cattle with mad cow disease and patients with variant Creutzfeldt-Jakob disease (vCJD).

Prion

About Prion Diseases

pirons

Prion diseases or transmissible spongiform encephalopathies (TSEs) are a family of rare progressive neurodegenerative disorders that affect both humans and animals. They are distinguished by long incubation periods, characteristic spongiform changes associated with neuronal loss, and a failure to induce inflammatory response.

The causative agent of TSEs is believed to be a prion. A prion is an abnormal, transmissible agent that is able to induce abnormal folding of normal cellular prion proteins in the brain, leading to brain damage and the characteristics signs and symptoms of the disease. Prion diseases are usually rapidly progressive and always fatal.

These diseases

  • are transmissible — from host to host of a single species and, sometimes, even from one species to another (such as a laboratory animal)
  • destroy brain tissue giving it a spongy appearance

For these reasons, prion diseases are also called transmissible spongiform encephalopathies or TSEs.

Examples

Creutzfeldt-Jakob Disease (CJD)

A number of humans have acquired CJD through accidental exposure to material contaminated with CJD prions.

  • Grafts of dura mater taken from patients with inherited CJD have transmitted the disease to more than 100 recipients.
  • Corneal transplants have also inadvertently transmitted CJD.
  • Instruments used in brain surgery on patients with CJD have transmitted the disease to other patients. Two years after their supposed sterilization, these instruments remained infectious.
  • Over 100 people have acquired CJD from injections of human growth hormone or human gonadotropins prepared from pooled pituitary glands that inadvertently included glands taken from humans with CJD.

Now that both hGH and human gonadotropins are available through recombinant DNA technology, such disastrous accidents need never recur.

Variant Creutzfeldt-Jakob Disease (vCJD)

mad-cow1

This human disorder appeared some years after the epidemic of BSE (Mad Cow Disease) swept through the cattle herds in Great Britain. Even though the cow and human PRNP genes differ at 30 codons, the sequence of their prions suggests that these patients (155 by 2005) acquired the disease from eating contaminated beef.

All the patients are homozygous for the susceptibility polymorphism of methionine at position 129.

The BSE epidemic has waned, and slaughter techniques that allow cattle nervous tissue in beef for human consumption have been banned since 1989. Now we must wait to see whether more cases of vCJD are going to emerge or whether the danger is over.

http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/P/Prions.html#CPEB

http://www.cdc.gov/ncidod/dvrd/prions/index.htm

http://www.bioedonline.org/news/news.cfm?art=702

Cute origins,scary virus

http://www.primatefreedom.com/images/mangabey.jpg 

Isn’t the monkey cute? It is a Sooty Mangabey. Bet you’re wondering what has it got to do with microbiology.
Well, make a guess? From the title of the post, it must have something to do with a virus.

The virus is the Human Immunodeficiency virus(HIV)! The HIV’s origin was this innocent looking monkey.

During the 20th century, non-human primates in sub-Saharan Africa transferred the virus to humans.

Both HIV-1 and HIV-2 were said to be mutated from the Simian Immunodeficiency Virus (SIV) from the Sooty Mangabey.

The HIV-1 is more virulent, thus it is easily transmitted and is the cause of the worldwide spread of HIV.

HIV-2 is less virulent and is contained in West Africa.

That’s enough about how it all started. Now, let’s understand what it does to our bodies.

The HIV is a lentivirus that can lead to acquired immunodeficiency syndrome (AIDS), a condition in humans in which the immune system begins to fail, leading to life-threatening opportunistic infections. A HIV patient needs different types of medication to suppress the virus to prolong their lives. The information below will allow you to understand why.

HIV attacks specific lymphocytes called T-cells (CD-4), takes them over, and multiplies. This destroys more T-cells, damaging the body’s ability to fight them off.

 

t-cell1

http://kidshealth.org/parent/infections/std/hiv.html

When the levels of T-cells are very low, HIV patients are more susceptible to other infections. This weakened immune deficiency is known as AIDS and would result in severe life-threatening infections, some forms of cancer, and the deterioration of the nervous system.

However, HIV can be controlled by drugs. Firstly, the viral attachment can be blocked by a class of drugs called entry inhibitors. This prevents the HIV from attacking the T-cell which prevents the reproduction of HIV. If HIV is attached, the HIV and T-cell would fuse. Drugs called entry or fusion inhibitors are used to block the fusion.

In order for HIV to reproduce, the RNA from the HIV has to be converted to DNA. Drugs called reverse transcriptase inhibitors block HIV’s reverse transcriptase from using these building blocks. These drugs contain faulty imitations of proteins found in a T-cell’s cytoplasm. The imitation building blocks in NRTIs are inserted into the DNA, preventing the double strand of DNA from becoming fully formed.

The enzyme protease allows the HIV’s material to be separated so they can be reassembled to new HIV. Drugs called such as Kaletra, Crixivan, and Viracept bind to the protease enzyme and prevent it from separating, the HIV subunits.

Enveloped DNA viruses

Enveloped DNA viruses

Virus Family

Virus Group

Disease Produced

Poxvirus

Variola Virus

Vaccinia Virus

Smallpox

Cowpox

Herpes Virus

Family

Herpes Simplex Type 1 (HSV-1)

Herpes Simples Type 2 (HSV-2)

Varicella-Zoster Virus (VZV)

Epstein-Barr Virus (EBV)

Herpesvirus- 8 (HV-8)

Cold Sores

Genital Herpes

Varicella (Chickenpox) and

Shingles (Zoster).

Infectious Mononucleosis

Burkitt Lymphoma and

Nasopharyngeal carcinoma.

Kaposi Sarcoma

Hepadnavirus

Hepatitis B Virus (HBV)

Hepatitis B

Herpes simplex virus 1

Also called as oral-facial herpesansmission: kissing or sharing drinking utensils

Herpes simplex virus 2

Also called as genital herpes

Transmission: sexual contact

Prevention: Don’t kiss and stop risky behaviours.

c22

http://www.entusa.com/oral_photos.htm

c31

Hepatitis B

Signs and symptoms: malaise, fever, chills, anorexia, abdominal discomfort, jaundice, dark urine, and diarrhoea.

Complete liver regeneration and restored liver function occur in most patients. However, about 10% of patients develop chronic liver disease in the form of cirrhosis (permanent liver scarring and loss of tissue). People with chronic hepatitis B are more likely to develop liver cancer.

Transmissions: sharing of contaminated needles and homosexual contact

Prevention: vaccines and avoid risky behaviours

c7

http://www.herbalprovider.com/imgs/yahoo/fatty-liver-hepatitis.jpg

c8