Making Mischief

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    Making Mischief 

    Viruses that infect bacteria are bacteriophages, or just phages. Their life history may include

    up to two cycles (figure 16.7). The lytic cycle, as the name suggests, ends when the bacterium

    lyses, or ruptures. t starts when the !irus attaches to the surface of the bacterium and injects

    its genome, and this genome, free in the cytoplasm, confiscates the cell machinery to

    replicate and assemble multiple copies. The thousands of new copies of the !irus burst from

    the host bacterium to find new bacteria to infect and, so, "uic#ly proliferate. n the lysogenic

    cycle, bacteriophages do not #ill the cell they infect, at least not right away. They inject their 

    genome, called a prophage, which then becomes integrated into the $%& of bacterium,

    replicating along with the bacterium as it replicates.

    Viruses that infect eu#aryotic cells may e'it peacefully, ta#ing some of the plasma membrane

    with them, or destructi!ely, causing deadly lysis of the cell. &lthough it has some

    idiosyncrasies, V is an e'ample of such a !irus, structurally resembling the flu or mumps

    !irus. V is a retro!irus, so named because instead of the transcription $%& *%&, it

    re!erses this flow of genetic information ($%&+*%&), starting with *%& that ma#es $%&.

    pon first infection of the cell, the *%& genome of V produces $%&, which enters the

    nucleus and becomes integrated, as a pro!irus, into the chromosomal $%& of the host cell.

    ere, the pro!irus acts, li#e any acti!e section of $%&, to synthesi-e products, in this case

    more !iral *%& and its associated proteins. These assembled new !iruses lea!e the cell to

    infect other cell (figure 16.)

    /y lysing cells, some !iruses directly #ill the host. V does not. nstead, V wea#ens the

    immune system of the host, a condition #nown as &$0. &t first, V enters and proliferatesin macrophages, cells that assist the immune system. ater, V enters critical cells of the

    immune system, the white blood cells #nown as T lymphocytes, where in the !irus multiplies,

    filling and e!entually lysing these cells as they e'it. &s the disease progresses, the e'ploding

    numbers of the !irus infect and gradually depopulate the body of T lymphocytes, lea!ing the

    indi!idual defenseless.

    ndi!iduals do not die directly from the disease, but indirectly, from a wea#ened condition

     produced by the !irus. 0o wea#ened, the indi!idual falls prey to passing opportunistic

    diseases or unchec#ed cancers that a healthy indi!idual might otherwise ward off. & slow

    death ensues.

    Evolving Plagues and Pathogens

    2ur future is li#ely to be a future of plagues. The body counts will be high because our 

    human population is at an all time high and growing. 3onsider just a few recent e'amples.

    The 4#iller flu5 of 11 tra!eled home with the soldiers of orld ar . orldwide, more

    than 81 million people died of this !irulent flu, many more than the numbers of soldiers who

    died in the war itself. The 4&sian 9lu5 of 1:7 spread around the world. n the nited 0tates

    alone, 1;;.;;; died, and many more were infected . The 4ong

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    :; million &mericans, 7;.;;; died. =ruptions of the =bola !irus in &frica can be particularly

    deadly. t spread through contact. ithin a few days of infections, symptoms may include

    high fe!er, stomach pain, bloody diarrhea, and !omit reddened by intestinal hemorrhage,

    death usually soon follows. ocal mortality rates can reach up to ; >. magine the

    conse"uences if this =bola !irus bro#e out of &frica and became a worldwide epidemic.