Biomedical Engineering Reference
In-Depth Information
using known or potentially infectious body fluids or tissues
and animals known to be or potentially infected with
LCMV; the same applies for the CH virus. LCMV may be
present in blood, cerebrospinal fluid, urine, nasopharyngeal
secretions, feces, and tissues of infected animals and
people. Parenteral inoculation, inhalation, and contamina-
tion of mucous membranes or broken skin with infectious
tissues or fluids from infected animals are common
hazards, and aerosol transmission of LCMV is well docu-
mented. Laboratory-associated infections associated with
LCMV-infected rodents are well documented, and natu-
rally occurring infections occur in nonhuman primates
(
Centers for Disease Control/National Institutes of Health,
2009
). Two zoo veterinarians who cared for CH-infected
callitrichids (at least one of whom was bitten by an infected
animal) were found to be seropositive for CHV, but
there was no development of clinical illness following
exposure.
This disease is important not only because it is lethal to
endangered species but also because a new type of
epidemic primate hepatitis appeared without warning.
Identification of the etiological agent showed that the
source was mice (Mus musculus), which are common in
zoos and are known to be hosts of LCMV (
Montali et al.,
1995
). Finding seropositive, asymptomatic personnel with
animal contact emphasizes the potential for transmission of
viruses from primate to human animals.
and chronic wasting syndromes now called SAIDS, oppor-
tunistic infections, necrotizing gingivitis, and retroperitoneal
fibromatosis (
Daniel et al., 1984; Marx et al., 1984, 1985;
Stromberg et al., 1984; Desrosiers et al., 1985
).
Species-specific simian foamy viruses (SFV) have been
found in primates ranging from prosimians to great apes,
and interspecies transmission has been documented
(
Leendertz et al., 2008
). Infection in primates is generally
asymptomatic. Antibodies against SFV have been found in
humans working closely with nonhuman primates, but
infections to date have been nonpathogenic (
Heneine et al.,
2003; Switzer et al., 2004; Khan, 2009
).
Lentiviruses are not oncogenic and characteristically
produce long-term, persistent infections that eventually
lead to chronic, debilitating diseases. This group includes
HIV, which causes acquired immune deficiency syndrome
(AIDS), and the simian immunodeficiency virus (SIV), as
well as the classic ungulate lentiviruses (Maedi-Visna virus
of sheep, caprine arthritis encephalitis virus, and equine
infectious anemia virus) plus lentiviruses from cats (
Ped-
ersen et al., 1987
) and cattle (
Gonda et al., 1987
). It should
be noted that SAIDS can be caused by both type D retro-
viruses and lentiviruses (
Benveniste et al., 1986; Daniel
et al., 1987, 1988
). These are distinctly different viruses so
it is important to determine which virus is being described
when reading the literature.
A number of SIV isolates have been obtained from
several species of nonhuman primates at various primate
facilities. Independent isolates of HIV and SIV vary from
one another to the extent that even independent isolates of
HIV-1 from the same individual can vary (
Hahn et al.,
1986
). From a biosafety standpoint, important features of
these viruses are their rate of mutation and the variability
produced within a given isolate by in vivo transmission
(
Kestle et al., 1988
). A striking example of this phenom-
enon was the production of a new virulent strain of the
sooty mangabey-derived SIV
SMM
by passage through a pig-
tailed macaque. The parent virus, which readily establishes
persistent infection in pig-tailed and rhesus macaques and
in sooty mangabeys, causes progressive AIDS-like disease
only in macaques. The new isolate (SIV
SMM-PBjl4
) infects
all three species and causes acute disease characterized by
bloody mucoid diarrhea and death within 12 weeks (
Fultz
et al., 1989b
). This demonstrates the potential for change in
these agents that could adapt them for human infection.
The different infectivity, morbidity, and mortality rates
in vivo, as well as different in vitro growth properties of
SIV isolates, determine the relative value of each as models
of HIV and optimal research use of each primate species.
Macaques infected with SIV are good models for testing
antiretroviral drugs because the effect on clinical illness
can be evaluated. Macaques can also be infected with HIV-
2, which is antigenically similar to SIV, and these species
are being used extensively for development of vaccines
Retroviral Diseases
The retroviruses are classified as type B, C, and D onco-
viruses, foamy viruses, and lentiviruses. All are of signifi-
cance in nonhuman primates, except the B type which is
represented by the mouse mammary tumor virus (
Desros-
iers, 1988
).
Type C oncoviruses include the murine, feline, and
avian leukemia and sarcoma viruses. The human T cell
leukemia viruses (HTLV-I and II), their simian counterpart
(STLV-I), and the bovine leukemia virus form a distinct
subgroup of type C oncoviruses. Type C oncovirus particles
were demonstrated by electron microscopy in neoplastic
tissues of a gibbon (Hylobates lar) with spontaneous
lymphosarcoma and in naturally occurring fibrosarcoma in
a woolly monkey (Lagothrix spp.). Experimental intra-
dermal inoculation of this woolly monkey-derived simian
sarcoma virus produced well-differentiated fibrosarcomas
in marmosets (
Rabin, 1978
).
The prototype of type D oncoviruses is the Mason
e
Pfizer monkey virus, which was isolated from a rhesus
monkey in 1969 (
Chopra and Mason, 1969
). This category
includes the feline leukemia virus and macaque type D
retroviruseswhich can produce a subclinical infection, slowly
developing tumors, and immunosuppression. Simian retro-
viruses (SRV) have been associated with immunodeficiency
