Bud’s FIV FAQs
1. What is FIV?
2. How do you know your cat has FIV?
3. How does FIV differ from AIDS?
4. How does FIV compare to HIV?
5. How well understood is FIV?
6. Is all FIV alike?
7. How does FIV do its damage?
8. Can FIV infection be prevented?
1. What is FIV?
Many people whose cats don’t have FIV (Feline Immunodeficiency Virus), and most people
who don’t have cats, have never heard of the disease. FIV is the feline version of HIV. It is a
lentivirus (i.e., slow-acting virus) of the type called a retrovirus (i.e., a virus whose RNA is converted to DNA for insertion into host genomic DNA). Cats frequently spread the
infection through bite wounds. For this reason, free-roaming outdoor cats–especially
unneutered males, who incline to fight over territory–are at greatest risk. Since Bud was an
abandoned stray when very young, this is the presumed route of his infection. FIV can also be
acquired through sexual contact (either vaginally or though sexually-motivated biting) or from a
mother before or after birth. It is a commonplace that mother-to-kitten transmission (“vertical transmission”) is not usual. Reputable sources, however, paint a mixed picture. According to one study,
FIV is transmitted from mother to young quite readily in utero, although establishment of actual
post-partum infection is less common. Another study reported a transmission rate of 22%. A
third states that if the mother is infected when already pregnant, productive infection of the
young is about ten times more likely. A new study concludes that laboratory models overstate
the frequency of maternal transmission in the wild. Lactation is another potential route of maternal infection. One
study found more virus per unit of volume in milk than in plasma. In summary, vertical transmission, while not as common as peer-to-peer (“horizontal”) transmission, is underestimated when characterized as “rare”. After the more usual (horizontal)infection, a brief period of illness ensues, characterized by several days of fever, neutropenia (a deficiency of neutrophils, a type of white cell) that may last for several months, and swelling of lymph nodes (lymphadenopathy) that may last up to nine months. Then the initial infection
subsides. Although some damage has already been done, to all outward appearances the cat
regains its original health. However, there is no true latency period.. A long, low-level battle
goes on at the cellular and intracellular level (largely in the lymphatic system) until the cat
finally becomes symptomatic.
2. How do you know your cat has FIV?
The standard test for FIV is an ELISA (Enzyme-Linked Immunosorbent Assay) that tests for
Feline Leukemia Virus, as well. For FIV, the test,according to validation studies, is about 95% accurate when the reading is definite, 80% or less when less-than-definite readings are included; false readings are most
often in the direction of the positive. A positive test, therefore, means a cat “probably” has
FIV, although false positives are more common than the aforementioned statistics imply. A cat owner should insist that any positive ELISA is confirmed by a follow-up test called
a Western Blot Electrophoresis test, which is more reliable with regard to false positives.
Another test called an IFA (Immunofluorescence Assay) is regarded in some areas of the world as an acceptable
confirming test. However, because both tests look for antibodies of FIV rather than the virus
itself, three circumstances may fool them. One is if an animal has only recently been infected. As
long as six to eight weeks may be required before antibodies appear in the bloodstream.
Another instance involves kittens born to infected queens. Often the kitten will test positive
because the mother has passed on her antibodies, not her virus. Three to six months may have to
pass before an uninfected kitten tests negative. A recent study found that three months are
sufficient, although anecdotal reports have claimed positive to negative antibody status
after as much as a full year. Any cat testing positive at three months should be given the benefit of the doubt and retested at six. The last circumstance is prior immunization with the FIV vaccine (see item 8 below). The only test that looks for the presence of virus is the PCR
(Polymerase Chain Reaction), which uses engineered copies of sections of virus that bind
biochemically to their viral counterpart in order to determine the presence, type, or number of
virus. Mass PCR testing for FIV continues to improve in reliability, though some labs are better than others. A positive result at the better labs is reliable. False negatives, however, do occur. For a complete discussion of the uses and limits of various FIV tests and how to approach problem situations, click here (“Understanding and Applying FIV Testing”). Bud tested
positive on the ELISA at age two. The result was reconfirmed by Western Blot many years later
(at age 10) because a skeptical parasitologist was “sure” he wouldn’t have survived that long
with FIV. Bud also had PCR testing to assess his viral load (See “Outcomes”).
3. How does FIV differ from AIDS?
AIDS is the final stage of infection with the Feline Immunodeficiency Virus. The lapse of time
between initial infection and emergence of FIV-related symptoms is variable. Some cats go 8 to 10 years or
longer before showing any symptoms at all, although the average has been placed closer to 5. According to one study, ten years old was the median age of cats with “AIDS-like disease.”
A number of factors may explain why some cats develop the disease more quickly than others, although there may be others that are still not entirely understood. Kittens infected
with the disease by their mother have, on average, a shorter life to look forward to than do cats infected when mature. However, there is no such thing as an “average” cat. For a complete discussion of variables known or suspected to determine FIV disease progression, click here (“Contributing Causes of FIV Disease Progression.”)
Bud, though already FIV + at age 2 when first encountered as a stray, did not become clearly symptomatic
until age 9. Following HIV-staging practice, an intermediate stage called ARC (AIDS-Related Complex) is sometimes used with
FIV, to define the period between the onset of symptoms of impaired immune
function and the more devastating immune-deficiency of the terminal stage. The term is a loose fit at best for FIV. ARC stage is usually said to be characterized by infections of the oral cavity and/or the upper respiratory tract, diarrhea, and
sometimes intermittent fever and weight loss. The AIDS label in HIV infection is conferred
according to the number of the specialized cells whose degradation by the virus is most directly
related to lost immunity or according to AIDS-defining illnesses such as Kaposi’s sarcoma or
thrush, illnesses almost always found only in instances of severe immune suppression. Cats have
no obvious equivalents of these illnesses, and the relevant specialized cell testing is not widely
available. Therefore the point at which the AIDS label is technically warranted is more difficult
to fix. Any combination of the following may characterize end-stage illness: persisting low red and/or white cell/differential counts, unexplained wasting, “failure to thrive,” organ failure, opportunistic infections, retinal degeneration, poor response to antibiotics, and fever. It has been estimated that only about three in ten cats with FIV will actually progress to AIDS, although FIV may nevertheless play a role in whatever condition ultimately leads to their demise. Bud’s illness may
never have reached the AIDS stage, although he registered serious effects from his
infection for a number of years and was highly immune-suppressed at the very end of
his life because of cancer.
4. How does FIV compare to HIV?
FIV and HIV are very similar illnesses–so similar that cats with FIV are routinely used to
advance the cause of HIV research. Each year thousands of cats are deliberately infected with the
FIV virus in order for researchers to study the minute inner-workings of the disease and to test
therapeutic agents. (Many therapeutic agents effective against HIV are also effective against FIV
and vice versa, but this is by no means always the case.) Some geneticists believe that FIV is an
older disease than HIV, having existed as long as three to six million years years. One geneticist
has theorized that FIV at some point in the distant past evolved from a bovine immunodeficiency
virus, then later “jumped” the species barrier to apes and became SIV, which in turn “jumped” to
humans and became HIV. Although a university lab worker may have been infected with a
(possibly engineered) strain of FIV, the virus is not believed to be transmissible to humans under
ordinary circumstances. A number of particular differences between the diseases exist. Cats, for
instance, have enough virus in their saliva to spread the disease; humans, it is generally felt, do
not. Conversely, sexual transmission is not a major feature of FIV, as it is of HIV (although it
does occur.) There are also differences at the genetic and biochemical levels. Genetically, FIV is
said to be better adapted to its host than HIV and, if not simpler in its structure, then less
specialized. FIV comprises the same structural and enzymatic genes (see top of page, left) as HIV, but lacks a number of accessory genes coding for individual proteins with specialized functions: TAT
(“Transactivator of transcription,” an accelerator of viral transcription), VPR (“Viral protein R,”
a regulator of nuclear import), NEF (“Negative regulatory factor,” a regulator of host immune
cell activation) and VPU (Viral protein U,” a regulator of new-virus release). FIV has a multi-purpose gene-like construct called Orf-A (“Open Reading Frame A”), which has been intensively
studied, but is not completely understood; it seems to include some actions of both the “missing”
HIV TAT gene and of several other specialized genes, as well. Biochemically, HIV and FIV
coopt receptors for many similar host immune-signaling proteins (“chemokines”) to achieve cell penetration, but the primary FIV
cooptee (or “co-receptor”), CXCR4, is a secondary one for HIV until a late stage of infection,
whereas CCR5, the primary cooptee for HIV, is (along with CCR3) a co-receptor in only some
strains of FIV, where it seems to enhance the expression of the primary co-receptor. Recently, it
has been discovered that the FIV viral envelope binds to a surface molecule of CD4+ cells called
CD134 and not to the CD4 molecule itself, as does HIV. These are isolated examples. FIV is
generally regarded as a less devastating disease than HIV with a more favorable prognosis because strains have a wider
divergence of virulence and disease expression is more variable. Although lab studies give the
impression that eventually FIV will be fatal, many people report FIV+ cats living a normal life
span and succumbing to other problems perhaps not directly related to their FIV.
5. How well understood is FIV?
The level of ignorance in the veterinary community about FIV has sometimes been shocking. Some vets continue to overestimate the ease of transmission, treating cats with FIV like lepers in the office and advising absurd degrees of sterility to protect other cats within the home, as if it were readily spreadable like distemper by surface contamination or like feline leukemia by casual interaction. Others over- or underestimate the prognosis for FIV+ cats, failing to understand the many variables that affect disease expression. Because of the kinship to HIV, FIV and the disease it causes have been studied extensively. Researchers have long realized that understanding the points of likeness and difference between HIV and FIV can be of great importance in understanding the human disease. This kinship has been a mixed blessing. On the negative side, thousands of cats have been deliberately infected and sacrificed in order to study the minutest of points. Particularly unfortunate is the fact that researchers have stacked the deck, more often than not, by consciously choosing viral strains of Known (and more HIV-like) pathogenicity and introducing them in amounts and by routes (notably parenteral injection) that bypass immune defenses that come into play with natural infection. The result has been to generate a grimmer overall disease profile than real-world experience warrants. On the other hand, no one ever would have invested the time and money that have been given over to FIV research had the similarity to HIV not existed. Although much remains to be understood about both diseases, the many millions of dollars spent in an attempt to understand and treat HIV have done much to advance the understanding of FIV. And yet comparatively little knowledge gained about therapeutics has trickled down into veterinary medicine. When trials have occurred, the standards have often fallen short of those routinely demanded in human medicine.
6. Is all FIV alike?
No, there are five recognized strains of FIV virus, based on genetic variations within the viral envelope and designated A through E. (A possible F strain has been postulated based on isolates found in Texas that appear to have evolved from the B strain.) Some individual viruses have been known to defy classification. In one city alone (Munich, Germany) three different subtypes were found–and one which defied classification. Statistically, strains
(called “Clades”) A and B are most common worldwide, as they are in the United States. Generally,
Clade A is more common in the western U.S., B in the Eastern U.S. Since more than one strain of FIV can infect the same cat, the evolution of new, mixed viral types through recombination can and does happen. Clade B is thought to be
the oldest of the common subtypes, the most genetically diverse, and the one best adapted to its
host. On average, Clade B runs higher viral loads than Clade A. Interestingly, in one study Clade
B showed higher viral loads than Clade A when the route of infection was intravenous, but the
results reversed when the route was transmucosal. So different virus types do have different
disease dynamics. Bud’s virus was Clade B, but defied distinct characterization for some time
when subjected to PCR testing. Subtypes–particularly B–have a great deal of diversity in their
genetic structure, because FIV is a highly unstable virus, though its rate of mutation is less than
that of HIV. More than half of all feline species have been found to have FIV antibodies,
although only housecats are believed to develop AIDS. (The status of lions and cheetahs, in this regard, is somewhat controversial.) The reason, it has been theorized, is that the virus has existed long enough in the wild population for natural selection to confer some level of tolerance.
7. How does FIV do its damage?
For a long time, a cat with FIV is able to manufacture enough replacements for the cells it is losing (most notably a type called a T4, or CD4+, lymphocyte) to keep its immune system
functioning at an adequate level. But eventually it cannot. The particularly devious character of
FIV disease is that the virus can use the immune system against itself in many ways. The inability
to clear the virus keeps the immune system chronically activated (virus can only enter the nucleus
of an activated cell); in the process, many uninfected cells are likewise lost to a “mistaken”
application of the immune system’s own internal controls (“apoptosis,” or programmed cell
death). “Turnover” of lymphocytes in their normal cycle increases. At varying rates depending
on the specific strain, the virus mutates to become more efficient in the use of its co-receptors,
accelerating its infectivity and broadening its reach to cell-types previously more difficult to
infect. Eventually, inflammation- and activation-induced fibrosis causes breakdown in the architecture of the lymph nodes, the thymus, and the gut lymphoid compartments that are home to a majority of the body's CD4+ cells, leading to immune insufficiency that is no longer directly linked to viral replication. When CD4+ lymphocytes particularly fall below
a threshold level or when they and other cells of the immune system become too poorly reactive
(“anergic”), the cat becomes liable to diseases he would otherwise not have caught. However, the
broad skewing of immune response as a result of viral infection is also a major feature of the
disease, exposing the cat to a variety of inflammatory diseases. Either excessive immune activity,
decreased tumor surveillance, or both heighten suscepability to certain cancers. Many centers of
FIV study report FIV-related cancer as the most common cause of mortality among their long-term populations, often in cats as yet showing minor or no FIV-related symptoms. (To view the “FIV and Lymphoma” page click here)
8. Can FIV infection be prevented?
The best prevention is to keep a cat indoors. An FIV vaccine (Fel-O-Vax) has been recently
introduced which confers substantial, but not complete, protection against infection. The vaccine
is a dual-type, made from A and D Clade subtypes. Although there was initial concern that poor
protection would be provided against other subtypes, particularly Clade B, which is the most
common, studies suggest that the vaccine is effective against at least those strains of Clade B
tested. The mechanism of protection in such cases appears to be enhanced cell-mediated
immunity, not antibody production. One virulent strain resistant to the vaccine has been noted by U.K. researchers (ironically, given the make-up of the vaccine, a Clade A virus), and European skeptics, particularly, complain of lack of testing against European field strains. Many people and vets fear that because inoculating a cat will cause it to test positive on an FIV antibody test, the cat might be euthanized if it found
its way into a shelter, where screening is routine. At this time there is no antibody test clinically available to distinguish true FIV+ cats from those vaccinated with Fel-O-Vax. (Unlike tests for feline leukemia virus, tests for FIV must look for antibodies, not viral antigen.) PCR testing can make the distinction, although, as previously stated, laboratories vary in reliability, and negative findings cannot be considered completely reliable. A vaccine-discriminant Elisa antibody test has been developed in Japan, with confirming tests done at the University of Florida. However, despite study data having been shown to a number of U.S. manufacturers, none as yet has picked it up to produce commercially. Yearly vaccine boosters are necessary, and vaccine-site sarcoma also remains a remote possibility. Since FIV is not easily transmissible, some people prefer not to vaccinate friendly indoor cats in households of mixed FIV+ and FIV- cats. (To view the “Casual Transmission of FIV?” page click here)
[Page Top]
