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originally posted by: intrptr
a reply to: soficrow
RE: "In West Africa, pigs commonly dig up Ebola victims' graves. Thing is, pigs catch Ebola and worst of all - Ebola transmission in pigs is airborne."
Talk about vectoring.
....I can't even imagine what other scenarios like this might be undiscovered as yet. ...
Birds fly a long ways on migrations, for instance. I wonder if the vultures can get it from carrion like dead pigs that get it from like dead humans? ...
Fruit bats: Africa’s greatest mammal migration
Forget the wildebeest of the Serengeti – Africa’s greatest mammal migration involves 8 million animals and takes place in the air.
….The bats are frequently attacked by birds of prey, such as fish eagles, while crocodiles snap up any unfortunate individuals that fall to the forest floor.
….In the 1980s, DW Thomas of Aberdeen University used sightings to estimate that these mammals travelled some 1,500km during the course of a year. But when Heidi monitored their movements, she discovered this to be a major underestimation.
She fitted four individuals with satellite-tracking collars, then plotted their movements on a map. She found that after their departure in December, her study bats had covered a whopping 1,000km in just one month. “They disappeared off the radar somewhere over the Democratic Republic of Congo (DRC),” says Heidi. “The collars could have been lost or damaged, or the bats eaten.”
However, previous data showed that one particular bat, named Hercules, had travelled 1,900km in six months. The DRC may not even have been his final destination – with a return trip to Kasanka later in the year, Hercules would have made a round trip of at least 3,800km, a staggering distance. The full route will not be known until more tracking studies are carried out.
Also wondering if mosquitos can spread it like malaria?
1 However, laboratory work indicates mosquitoes are unlikely to be transmitters of Ebola virus.
Viruses that cause haemorrhagic fevers are transmitted by mosquitoes (dengue, yellow fever, RVF), ticks (CCHF), rodents (Hantavirus, Lassa) or bats (Ebola, Marburg). For Ebola and Marburg viruses, humans have been infected from contact with tissues of diseased non-human primates (monkeys and apes) and other mammals, but most human infections have resulted from direct contact with the body fluids or secretions of infected patients. Humans who develop CCHF usually become infected from a tick bite but can also acquire the virus from direct contact with blood or other infected issues from livestock or from infected patients. RVF can be acquired either by mosquito bite or by direct contact with blood or tissues of infected animals (mainly sheep), including consumption of unpasteurized milk. Lassa fever virus is carried by rodents and transmitted by excreta, either as aerosols or by direct contact. Some viral haemorrhagic fevers have been amplified in hospitals by nosocomial transmission resulting from unsafe procedures, use of contaminated medical devices (including needles and syringes) and unprotected exposure to contaminated body fluids.
The enigma surrounding the natural transmission cycles of Ebola (EBO) and Marburg (MBG) viruses remains a challenge for scientific research. Since my charge in preparing this paper was to present hypotheses, to stimulate nonlinear thinking, and to suggest new avenues for investigation, what follows is speculation, extrapolation, and conjecture. The reader should keep in mind that certain hypotheses may not be consistent with the prevailing views of some filovirologists.
An interesting possibility is that filoviruses may be arthropod or plant viruses, with non—blood-feeding arthropods transmitting the virus to intermediate hosts or humans during oral ingestion or envenomation. Paradoxically, in Africa, Ebola virus disease has high lethality and high seroprevalence as determined by the IFA test. If the seroreactivity is confirmed by more specific tests, then the Ebola virus serogroup in Africa probably contains an antigenically cross-reactive, enzootic, nonpathogenic agent(s). Such viruses may have separate life cycles or may give rise to virulent strains by mutation.
A possible explanation for the infrequent emergence of virulent EBO strains is that these viruses arise by gradual or stepwise mutation from an “enzootic” virus rather than being sustained in a cryptic maintenance cycle. The analog in arbovirology is the alphavirus, Venezuelan equine encephalitis, which is transformed by stepwise mutation from a nonpathogenic enzootic virus (ID subtype) to a virulent epizootic virus (IC subtype) having a different range of vectors and hosts . Single-site mutations can give rise to profound shifts in virulence. Variants of rabies virus selected by monoclonal antibodies  or chemical mutagenesis [56) were found to be nonpathogenic on the basis of a specific, single amino acid change (arginine to glutamine) at position 333 in the G protein. It is possible that a single-site mutation or a few stepwise mutations could explain the sudden conversion of a nonpathogenic to a virulent EBO strain.
Bats (particularly solitary microchiropteran species) are leading contenders as reservoir hosts. Virus transfer to humans occurs by contact with the primary reservoir or via an intermediate animal that acquired infection from the reservoir and is, in turn, hunted by humans.
As will be pointed out later, it is possible that the filoviruses represent a diverse complex of agents with different transmission cycles, as is the case for the lyssavirus and vesiculovirus genera, raising the difficulty of interpreting heterologous cross-reacting antibodies. Virulent strains of EBO and MBG virus may not persist in a local reservoir but rather cause wandering epizootics that return at long intervals to any one location. It is also possible that the virulent filovirus strains do not have sustained transmission cycles at all but arise from time to time by mutation from enzootic variants.
The susceptibility to infection of arthropod taxa can be assessed by virus replication after intrathoracic inoculation of virus. Turell et al.  reported that EBO virus, subtype Reston (EBO-R), failed to replicate in Culex or Aedes mosquitoes and in Ornithodoros ticks. However, Kunz et al.  previously reported that MBG virus could persist in Aedes mosquitoes for 3 weeks or more, indicating that certain arthropods exposed towasp.Altho the virus could be transient or persistent carriers of infection. Many potential blood-feeding arthropod vectors (phlebotomine flies, culicoids, ixodid ticks, mites, fleas, and wingless flies associated with bats) have not been tested by experimental inoculation. The susceptibility of insects used by humans or wild vertebrate reservoir hosts as a source of food (including termites, moths, and larvae [grubs]) also has not been explored. As will be discussed below, there has been recent speculation about the possible role of leafhoppers in filovirus ecology; therefore, experimental studies should determine the host range of EBO virus for plant-feeding bugs.
EBO and MBG viruses are similar in genome organization and have extensive sequence homology but do not share cross-reactive antigens . The ecology of EBO viruses is certainly more complex than that of MBG. Operational hypotheses on the ecology of EBO virus must take into account the factors discussed below.
At least 4 genetic subtypes of EBO virus have been recognized: Zaire (EBO-Z), Côte d'Ivoire (EBO-CI) , Sudan (EBO-S) , and EBO-R. EBO-R was recovered in the Philippines  and from monkeys imported from the Philippines to the United States and Europe.
The occurrence of a distinct EBO virus subtype in the Philippines has important implications for filovirus ecology, since it implies that EBO group viruses may have been carried by migratory hosts at some point in their evolution.
In other words what shows up as Ebola in humans, might not be Ebola in other animals, but is something else that mutates into ebola and then appears in humans.