Microbiology and Immunology

WORLD OF MICROBIOLOGY AND IMMUNOLOGY Hemorrhagic fevers and diseases

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ties in the infectious ability of the virus. Indeed, hemagglu-

tinin is the major virulence (disease-causing) factor of the

influenza virus.

There are three distinct haemagglutinins important in

human infections that are encoded by genes in the virus. These

are designated as H1, H2, and H3. Animal influenza viruses

contain nine additional types of hemagglutinin.

Neuraminidase is the common name for acetyl-neu-

raminyl hydrolase. The glycoprotein compound is an enzyme.

The enzyme removes residues called N-Acetyl-neuraminic

acid from chains of sugars and from other glycoproteins. The

disruption of the neuraminic acid residues allows the virus to

both pass out of the human epithelial cells in which it is repli-

cating, and enter new cells to initiate a new round of viral

replication. The activity of neuraminidase disrupts the mucous

fluid that is present in the respiratory tract. Also, possession of

neuraminidase keeps the viruses from aggregating with other

virus particles. The result of these activities is to ease the

spread of the virus through the respiratory tract.

Two different species of neuraminidase, designated N1

and N2, are important in human infections, while seven addi-

tional species are important in animal influenza viruses.

Inhibitors of neuraminidase have been developed in an

effort to thwart the viral infection. The inhibitors are struc-

turally similar to the silica acid on the surface of human

epithelial cells. The rational is that the virus will bind to the

inhibitor rather than to the human cells, and the inhibitor-viral

complex can be removed from the body.

Hemagglutinin and neuraminidase are used in the des-

ignation of the different antigenic types of the influenza virus

that have and continue to appear. For example, Influenza

A/Taiwan/86/H1N1 is an influenza A strain of the H1 hemag-

glutinin type and N1 neuraminidase type that was first isolated

in Taiwan in 1986.

Both hemagglutinin and neuraminidase tend to

undergo what is termed antigenic drift, which is a slight but

frequent change in the antigenic character. The slight change

is still usually enough to thwart the recognition capabilities

of the immune system. Hence, annual vaccinations are nec-

essary to minimize the chance of acquiring an influenza

infection. A major antigenic change in one or both of the gly-

coproteins, as happened in the 1918 virus, is termed anti-

genic shift.

See alsoFlu, the great flu epidemic of 1918; Mutations and

mutagenesis

HEMOLYSIS AND HEMOLYTIC REACTIONS

• seeBLOOD AGAR, HEMOLYSIS, AND HEMOLYTIC REACTIONS

HEMOLYTIC REACTIONS•seeBLOOD AGAR,

HEMOLYSIS, AND HEMOLYTIC REACTIONS

HHemorrhagic fevers and diseasesEMORRHAGIC FEVERS AND DISEASES

Hemorrhagic diseases are caused by infection with virusesor

bacteria. As the name implies, a hallmark of a hemorrhagic

disease is copious bleeding. The onset of a hemorrhagic fever

or disease can lead to relatively mild symptoms that clear up

within a short time. However, hemorrhagic diseases are most

recognized because of the ferocity and lethality of their symp-

toms as well as the speed at which they render a person

extremely ill.

Virtually all the hemorrhagic diseases of microbiologi-

cal origin that arise with any frequency are caused by viruses.

The various viral diseases are also known as viral hemorrhagic

fevers. Bacterial infections that lead to hemorrhagic fever are

rare. One example is a bacterium known as scrub typhus.

The viruses that cause hemorrhagic diseases are mem-

bers of four groups. These are the arenaviruses, filoviruses,

bunyaviruses, and the flaviviruses. Arenaviruses are the cause

of Argentine hemorrhagic fever, Bolivian hemorrhagic fever,

Sabia-associated hemorrhagic fever, Lassa fever,

Lymphocytic choriomeningitis, and Venezuelan hemorrhagic

fever. The Bunyavirus group causes Crimean-Congo hemor-

rhagic fever, Rift Valley fever, and Hantavirus pulmonary syn-

drome. Filoviruses are the cause of Ebola hemorrhagic fever

and Marburg hemorrhagic fever. Lastly, the Flaviviruses cause

tick-borne encephalitis, yellow fever, Dengue hemorrhagic

fever, Kyasanur Forest disease, and Omsk hemorrhagic fever.

While the viruses in the groups display differences in

structure and severity of the symptoms they can cause, there

are some features that are shared by all the viruses. For

instance, all the hemorrhagic viruses contain ribonucleic acid

as their genetic material. The nucleic acid is contained within

a so-called envelope that is typically made of lipid.

Additionally, all the viruses require a host in which to live.

The animal or insect that serves as the host is also called the

natural reservoir of the particular virus. This natural reservoir

does not include humans. Infection of humans occurs only

incidentally upon contact with the natural reservoir.

Hemorrhagic diseases can be devastating for the victim.

The symptoms can progress from mild to catastrophic in only

hours. As a result, an outbreak of hemorrhagic disease tends to

be self-limiting in a short time. In some cases, this is because

the high death rate of those who are infected literally leaves

the virus with no host to infect. Often the outbreak fades away

as quickly as it appeared.

Hemorrhagic fever related illnesses appear in a geo-

graphical area where the natural reservoir and human are both

present. If the contact between the two species is close

enough, then the disease causing microorganism may be able

to pass from the species that is the natural reservoir to the

human.

Although little is still clear about the state of the

microbes in their natural hosts, it is reasonably clear now that

the viruses do not damage these hosts as much as they do a

human who acquires the microorganisms. Clarifying the rea-

sons for the resistance of the natural host to the infections

would be helpful in finding an effective treatment for human

hemorrhagic diseases.

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