Can Yersinia effectors have the ability to regulate themselves to work with PAMPs? Can the Yersinia effectors be ever recognized as PAMPs by the host?

There have been recurring cases of mad-cow disease in the United Kingdom since the mid-1990s. Mad-cow disease is caused by a prion, an infectious particle that consists only of protein. In 1986, the media began reporting that cows all over England were dying from a mysterious disease. Initially, there was little interest in determining whether humans could be affected. For 10 years, the British government maintained that this unusual disease could not be transmitted to humans. However, in March 1996, the government did an about-face and announced that bovine spongiform encephalopathy (BSE), commonly known as mad-cow disease, can be transmitted to humans, where it is known as variant Creutzfeldt-Jakob disease (vCJD). As in cows, this disease eats away at the nervous system, destroying the brain and essentially turning it into a spongelike structure filled with holes. Victims experience dementia; confusion; loss of speech, sight, and hearing; convulsions; coma; and finally death. Prion diseases are always fatal, and there is no treatment. Precautionary measures taken in Britain to prevent this disease in humans may have begun too late. Many of the victims contracted it over a decade earlier, when the BSE epidemic began, and the incubation period is long (vCJD has an incubation period of 10 to 40 years). A recent study concluded that 1 in 2,000 people in Great Britain carry the abnormally folded protein that causes vCJD. In spite of these numbers, the death rate from vCJD remains low. It is not clear whether this means that the incubation period for the disease is much longer than previously thought, or whether they may never develop the disease. If you were traveling in Europe, would you eat beef? Give sound reasons why or why not.

What is the role of Agrobacterium tumefaciens in the production of transgenic plants? a. Genes from A. fume fociens are inserted into plant DNA to give the plant different traits. b. Transgenic plants have been given resistance to the pest A. tumefacaens. c. A. wmefaciens is used as a vector to move genes into plant cells. d. Plant genes are incorporated into the genome of Agrobacterium tumefaciens.

Which of these statements is true? An antibiotic is any substance produced by a organism that is antagonistic to the growth of prokaryotes An antibiotic is any substance produced by a prokaryote that is antagonistic to the growth of other viruses An antibiotic is any substance produced by a prokaryote that is antagonistic to the growth of eukaryotic cells An antibiotic is any substance produced by a prokaryote that prevents growth of the same prokaryote.

If you suspected that heterozygous carriers of a particular disease gene had a selective advantage in resisting a type of infection, how would you go about testing that hypothesis?

The Adaptive Immune Response Is a Specific Defense Against Infection In cystic fibrosis gene therapy, scientists propose the use of viral vectors to deliver normal genes to cells in the lungs. What immunological risks are involved in this procedure?

Figure 21.10 Which of the following statements is false? In the lytic cycle, new phages are produced and released into the environment. In the lysogenic cycle, phage DNA is incorporated into the host genome. An environmental stressor can cause the phage to initiate the lysogenic cycle. Cell lysis only occurs in the lytic cycle.

Arrange the following list into the correct sequence for part of the cycle of a retrovirus: 1. dsDNA integrated into host DNA 2.viral proteins synthesized on host ribosomes 3. viral DNA uses host enzymes to transcribe viral RNA 4. reverse transcriptase catalyzes synthesis of ssDNA 5. synthesis of second DNA strand (a) 5, 2, 1, 3, 4 (b) 5, 2, 3, 4, 1 (c) 4, 5, 1, 3, 2 (d) 4, 1, 2, 3, 5 (e) 2, 1, 3, 4, 5

There have been recurring cases of mad-cow disease in the United Kingdom since the mid-1990s. Mad-cow disease is caused by a prion, an infectious particle that consists only of protein. In 1986, the media began reporting that cows all over England were dying from a mysterious disease. Initially, there was little interest in determining whether humans could be affected. For 10 years, the British government maintained that this unusual disease could not be transmitted to humans. However, in March 1996, the government did an about-face and announced that bovine spongiform encephalopathy (BSE), commonly known as mad-cow disease, can be transmitted to humans, where it is known as variant Creutzfeldt-Jakob disease (VCJD). As in cows, this disease eats away at the nervous system, destroying the brain and essentially turning it into a spongelike structure filled with holes. Victims experience dementia; confusion; loss of speech, sight, and hearing; convulsions; coma; and finally death. Prion diseases are always fatal, and there is no treatment. Precautionary measures taken in Britain to prevent this disease in humans may have begun too late. Many of the victims contracted it over a decade earlier, when the BSE epidemic began, and the incubation period is long (VCJD has an incubation period of 10 to 40 years). A recent study concluded that 1 in 2,000 people in Great Britain carry the abnormally folded protein that causes VCJD. In spite of these numbers, the death rate from VCJD remains low. It is not clear whether this means that the incubation period for the disease is much longer than previously thought, or whether they may never develop the disease. How can a prion replicate itself without genetic material?

Adapting to Host Defenses Surface proteins called HLAs allow white blood cells to detect HIV particles and fight an infection. In a recent study, scientists tested whether HIV is adapting to this host defense. They did so by looking at the frequency of a specific mutation (1135X) in HIV. This escape mutation helps the virus avoid detection by a version of the HLA protein (HLA-B51) that is common in some regions of the world, but not in others. FIGURE 20.19 shows the percentage of HIV-positive people who had HIV with the 1135X mutation. Data were collected at medical centers from several parts of the world. FIGURE 20.19 Regional variation in the frequency of the 1135X escape mutation among HIV-positive people. For each region, pink bars represent the percentage of people whose blood cells have HLA-B51. and thus cannot detect 1135X mutants. Blue bars represent the percentage of people with other versions of the HLA protein. These people have blood cells that can detect and fight HIV even if it has the 1135X mutation. 4. Japan has a high frequency of HLA-B51; about half the population has it. How might this explain the high frequency of the 1135X mutation in Japanese with other HLAs?