December 13-14, 2001
concerns for Simian Foamy virus (SFV) transmission by Blood and Blood Products
viruses (FV), or Spumaviruses, belong to retroviridae family. The FV genome
encodes the canonical retroviral gag,
pol, and env genes, as well as at least two additional genes termed tas (bel-1)
and bet. FV was first described in
1954 when it was found to contaminate primary monkey kidney cell cultures. Soon
thereafter, FV was isolated from a wide variety of nonhuman primate species (1). The prevalence of FV infection in naturally
infected animals is generally high and varies widely depending on the species
and environmental condition (1). The
seroprevalence is generally high in animals housed in captivity compared to
animals in the wild. In 1971 a putative human FV was isolated from
nasopharyngeal carcinoma (NPC) from a Kenyan patient (2). However, further
analysis of the
so called human FV clone by several
investigators revealed that it is a variant strain of chimpanzee FV. The precise mode of transmission of FV
is not well understood. So f or the studies indicate that transmission can
occur through saliva.
Mechanism of FV pathogenesis
has been studied in several animal models such as
rabbits and mice (3, 4). Virus has been
recovered from various organs from such animals. No pathology was noted in any
FV-infected animals. A wide variety of diseases such as thyroiditis de
Quervain, Graves disease, multiple sclerosis, Myasthenia Gravis have been
tenuously associated with FV infection of humans (1). However, use of combination of
multiple assays (western blot, RIPA, IFA and PCR) for the
detection of the virus, failed to confirm either endemic human infection or the
association of disease with FV in humans. Because of no definite FV
pathogenesis, this virus has been dubbed as “ a virus in search of a disease” (5).
have also focused on determining whether specific human population is at risk
to be infected by FV. The outcome of several studies over a period of time has
shown that a significant number of people living in East and central Africa are
seropositive by more than one assay. Recent studies with nonhuman primate
handlers such as veterinarians and zookeepers have also indicated a small but
significant number (1.8- 3.0%) are seropositive (6, 7). There was neither
of disease s
nor sexual transmission of SFV in one of the stud y (7).
conclusion at present there is not enough evidence
for FV pathogenesis in
humans or transmission by blood.
Issue: On June 29, 2001
In May of this year, Health Canada researchers conducted an anonymous, unlinked
SFV surveillance study of individuals who work with non-human primates.
Indicative of SFV zoonosis, of the 46 participants tested, one serum sample
reacted strongly while another serum sample reacted weakly to SFV proteins
(western blot analysis). The
purpose of this study was to determine the risk of SFV infection in animal
handlers and to determine the impact, if any, on the
Canadian Blood supply. There also
was discussion by
Health Canada whether the employees handling nonhuman primates should defer
from donating blood, tissue or organs until more is known about the
pathogenesis of SFV. Subsequently, we had a teleconference with
scientists from Health Canada and CDC to discuss the issue of SFV transmission
from nonhuman primates to humans. As is evident from the
literature survey, there is no definite proof of SFV pathogenesis in
humans nor is as well as SFV transmission by blood. (7, 8)At present it
appears that there is insufficient data to exclude the risk of SFV transmission
by transfusion. Therefore, FDA in
consultation with CDC and Health Canada decided it would discuss the issue of SFV
pathogenesis in humans and transmission by blood to its to seek their
input. In addition, both
and FDA will present the outline of future studies in both monkeys and humans
to address the question of possible SFV transmission by blood. Based on the
outcome of these studies, FDA
in future will present the data to BPAC members and
at that time will seek their opinion about possible blood donor deferral of
nonhuman primate handlers.
the specific questions
we plan to seek opinion from the BPAC members.
Does the committee agree that the currently available data are insufficient to assess if SFV can
cause adverse health effects in humans?
the proposed studies adequate to evaluate SFV transmission
by blood ?
1. Meiering CD, Linial ML. (2001) Historical perspective of foamy virus epidemiology and infection. Clin Microbiol Rev. 14: 165-176.
2. Achong BG, Mansell PW, Epstein MA, Clifford P. (1971) An unusual virus in cultures from a human nasopharyngeal carcinoma. J Natl Cancer Inst. 46: 299-307.
3. Schmidt M, Niewiesk S, Heeney J, Aguzzi A, Rethwilm A. (1997) Mouse model to study the replication of primate foamy viruses. J Gen Virol. 78: 1929-1933.
4. Swack NS, Hsiung GD. (1975) Pathogenesis of simian foamy virus infection in natural and experimental hosts. Infect Immun. 12: 470-474.
5. Weiss RA. (1988) Foamy retroviruses. A virus in search of a disease. Nature. 333: 497-498.
6. Sandstrom PA, Phan KO, Switzer WM, Fredeking T, Chapman L, Heneine W, Folks TM. (2000) Simian foamy virus infection among zookeepers. Lancet. 355: 551-552.
7. Heneine W, Switzer WM, Sandstrom P, Brown J, Vedapuri S, Schable CA, Khan AS, Lerche NW, Schweizer M, Neumann-Haefelin D, Chapman LE, Folks TM. (1998) Identification of a human population infected with simian foamy viruses. Nat Med. 4: 403-407.
8. Schweizer M, Falcone V, Gange J, Turek R, Neumann-Haefelin D. (1997) Simian foamy virus isolated from an accidentally infected human individual. J Virol. 71: 4821-4824.