Microbiology and Immunology

WORLD OF MICROBIOLOGY AND IMMUNOLOGY Slow viruses

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The plasmodial slime molds are relatively common in

temperate regions and can be found living on decaying plant

matter. There are about 400 different species. Depending on

the species, the color of the amorphous cell mass, the plas-

modium, can be red, yellow, brown, orange, green, or other

colors. The color of the plasmodium and the morphology of

the reproductive body, the sporocarp, are used to identify the

different species.

The plasmodial slime molds are superficially similar to

the cellular slime molds. Both have a haploid amoeba phase in

when cells feed by phagocytosis, followed by a phase with a

large amorphous cell mass, and then a reproductive phase with

a stalked fruiting body.

However, the plasmodial slime molds are distinguished

from the cellular slime molds by several unique features of

their life cycle. First, the germinating spores produce flagel-

lated as well as unflagellated cells. Second, two separate hap-

loid cells fuse to produce a zygote with a diploid nucleus.

Third, the zygote develops into a plasmodium, which typically

contains many thousands of diploid nuclei, all surrounded by

a continuous plasma membrane.

The cytoplasmof the plasmodium moves about within

the cell, a process known as cytoplasmic streaming. This is

readily visible with a microscope. The function of cytoplas-

mic streaming is presumably to move nutrients about within

the giant cell.

In nature, plasmodial slime molds grow well in wet and

humid environments, and under such conditions the plasmod-

ium of some species can be quite large. After a particularly wet

spring in Texas in 1973, several residents of a Dallas suburb

reported a large, moving, slimy mass, which they termed “the

Blob.” One reporter in the local press speculated that the Blob

was a mutant bacterium, able to take over the earth.

Fortunately, a local mycologist soberly identified the Blob as

Fuligo septica,a species of plasmodial slime mold.

Another plasmodial slime mold, Physarum poly-

cephalum,is easily grown in the laboratory and is often used

by biologists as a model organism for studies of cytoplasmic

streaming, biochemistry, and cytology. The plasmodium of

this species moves in response to various stimuli, including

ultraviolet and blue light. The proteins actin and myosin are

involved in this movement. Interestingly, actin and myosin

also control the movement of muscles in higher organisms,

including humans.

See alsoMycology

SSlow virusesLOW VIRUSES

Historically, the term “slow virus infections” was coined for a

poorly defined group of seemingly viral diseases which were

later found to be caused by several quite different conven-

tional viruses, also unconventional infectious agents. They

nevertheless shared the properties of causing diseases with

long incubation periods and a protracted course of illness,

affecting largely the central nervous and/or the lymph system

and usually culminating in death. The slow virus concept was

first introduced by the Icelandic physician Bjorn Sigurdsson

(1913–1959) in 1954. He and his co-workers had made pio-

neering studies on slow diseases in sheep including maedi-

visna and scrapie. Maedi is a slowly progressive interstitial

pneumoniaof adult sheep while visna is a slow, progressive

encephalomyelitis and the same virus, belonging, to the

lentivirus subgroup of retroviruses, was found to be responsi-

ble for both conditions.

Since the original isolation of the maedi-visna virus,

concern with slow viral infections, both in animals and in

humans, has grown. Research on sheep lentiviruses and their

pathogenesis has continued to this day and received an impor-

tant impetus in the 1980s with the recognition of the devastat-

ing condition in humans known as acquired immunodeficiency

syndrome (AIDS). AIDS shared many of the attributes of slow

virus infections in animals and led virologists to suspect, then

to identify, the lentivirus causing AIDS: the human immunode-

ficiency virusor HIV. Questions posed by Bjorn Sigurdsson’s

work on maedi-visna also became the central pathogenic ques-

tions of HIV disease. For example: how and where does HIV

persist despite an initially robust and long-sustained immune

response? How does HIV actually destroy the tissues it infects?

Why do these events unfold so slowly? Final answers to all

these questions have still not been found and there is much

research still to be done on the lentiviruses but Sigurdsson’s

contribution to HIV research through the study of maedi-visna

is now recognized.

Other slow virus infections of humans due by conven-

tional viruses include progressive multifocal leukoen-

cephalopathy (PML) caused by the JC papovavirus. This is an

opportunistic infection in hosts that have defective cell-medi-

ated immunityand the majority of human cases now occur in

HIV 1 infected individuals. Patients present with progressive

multifocal signs including visual loss, aphasia (difficulty

speaking), seizures, dementia, personality changes, gait prob-

lems, and less commonly, cerebellar, brain stem, and spinal

cord features. Death occurs within weeks to months of clinical

onset. Subacute sclerosing panencephalitis (SSPE), another

slow infection, has been identified as a rare consequence of

chronic persistant infection by the measles(rubella) virus,

causing an insidious syndrome of behavioral changes in young

children. Patients develop motor abnormalities, in particular

myoclonic jerks, and ultimately become mute, quadriplegic,

and in rigid stupor. SSPE is found worldwide with a frequency

of one case per million per year. Progressive rubella panen-

cephalitis is another very rare slow virus infection of children

and young people caused by the same virus. Most patients

have a history of congenital or acquired rubella and the clini-

cal course is more protracted than in SSPE with progressive

neurologic deficit occurring over several years. A third slow

virus of humans that has had some publicity in recent years is

the human T-cell leukemia virus(HTLV) types 1 and 2 which

are associated with adult T-cell leukemia. It was initially

thought that the causative agent of AIDS was related to HTLV

though it later became clear that whereas HTLV 1 and 2 are

both oncogenic (“cancer producing”) retroviruses, HIV

belongs to the lentivirus sub-group.

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