Abstract
PROBLEM
Pediatric human immunodeficiency virus (HIV) infection is largely a result of transplacental transmission, and pregnancy perturbation is more frequent in HIV-infected women. Dysregulation of placental immunology may occur during HIV infection, possibly facilitating HIV vertical transfer and miscarriage. The (FIV)-infected cat is a useful small-animal model for HIV pathogenesis because the viruses share common biological and clinical features. Transplacental transmission is readily achieved experimentally, resulting in a high proportion of infected offspring and frequent reproductive failure.
METHOD OF STUDY
We are using this model to examine lentivirus-induced placental immunopathology to determine the role aberrant immunology plays in intrauterine transmission and pregnancy perturbation.
RESULTS
Kittens were cesarean delivered from FIV-B-2542-infected and control queens at week 8 gestation (1 week short of term), and placental and fetal specimens were collected. On average, control queens delivered 3.8 kittens/litter, and 1 of 31 kittens (3.2%) was non-viable. FIV-infected queens produced 2.7 kittens/litter with 15 of 25 fetuses (60%) non-viable. The virus was detected in 14 of 15 placentas (93%) and 21 of 22 fetuses (95%) using polymerase chain reaction (PCR). Using a one-step, real time reverse transcriptase (RT)-PCR, we measured expression of representative placental T helper 1 (Th1) cytokines, interleukin (IL)-1beta and interferon (IFN)-gamma, a Th2 cytokine, IL-10, and chemokine receptor CXCR4. A comparison of placental cytokine expression between infected and control queens did not reveal differences between the two groups. However, elevated expression of Th1 cytokines and increased Th1/Th2 ratios (IL-1beta/IL-10) occurred in placentas from resorptions, indicating that increased placental Th1 cytokine expression was associated with pregnancy failure in the FIV-infected cat.
CONCLUSION
The potential to establish efficient FIV in utero transmission, coupled with the parallels in immunopathology between FIV-infected cats and HIV-infected humans, suggests the usefulness of the FIV-infected cat as a cost-effective, small-animal model to study lentivirus-induced immunopathology, transplacental infection, and reproductive failure.
TY - JOUR
T1 - The feline immunodeficiency virus-infected cat: a model for lentivirus-induced placental immunopathology and reproductive failure (mini-review).
A1 - Coats,Karen S,
PY - 2005/9/2/pubmed
PY - 2006/7/15/medline
PY - 2005/9/2/entrez
SP - 169
EP - 85
JF - American journal of reproductive immunology (New York, N.Y. : 1989)
JO - Am J Reprod Immunol
VL - 54
IS - 4
N2 - PROBLEM: Pediatric human immunodeficiency virus (HIV) infection is largely a result of transplacental transmission, and pregnancy perturbation is more frequent in HIV-infected women. Dysregulation of placental immunology may occur during HIV infection, possibly facilitating HIV vertical transfer and miscarriage. The (FIV)-infected cat is a useful small-animal model for HIV pathogenesis because the viruses share common biological and clinical features. Transplacental transmission is readily achieved experimentally, resulting in a high proportion of infected offspring and frequent reproductive failure. METHOD OF STUDY: We are using this model to examine lentivirus-induced placental immunopathology to determine the role aberrant immunology plays in intrauterine transmission and pregnancy perturbation. RESULTS: Kittens were cesarean delivered from FIV-B-2542-infected and control queens at week 8 gestation (1 week short of term), and placental and fetal specimens were collected. On average, control queens delivered 3.8 kittens/litter, and 1 of 31 kittens (3.2%) was non-viable. FIV-infected queens produced 2.7 kittens/litter with 15 of 25 fetuses (60%) non-viable. The virus was detected in 14 of 15 placentas (93%) and 21 of 22 fetuses (95%) using polymerase chain reaction (PCR). Using a one-step, real time reverse transcriptase (RT)-PCR, we measured expression of representative placental T helper 1 (Th1) cytokines, interleukin (IL)-1beta and interferon (IFN)-gamma, a Th2 cytokine, IL-10, and chemokine receptor CXCR4. A comparison of placental cytokine expression between infected and control queens did not reveal differences between the two groups. However, elevated expression of Th1 cytokines and increased Th1/Th2 ratios (IL-1beta/IL-10) occurred in placentas from resorptions, indicating that increased placental Th1 cytokine expression was associated with pregnancy failure in the FIV-infected cat. CONCLUSION: The potential to establish efficient FIV in utero transmission, coupled with the parallels in immunopathology between FIV-infected cats and HIV-infected humans, suggests the usefulness of the FIV-infected cat as a cost-effective, small-animal model to study lentivirus-induced immunopathology, transplacental infection, and reproductive failure.
SN - 1046-7408
UR - https://www.unboundmedicine.com/medline/citation/16135008/The_feline_immunodeficiency_virus_infected_cat:_a_model_for_lentivirus_induced_placental_immunopathology_and_reproductive_failure__mini_review__
DB - PRIME
DP - Unbound Medicine
ER -
