Lymphocytic choriomeningitis is not a commonly reported infection in humans, though most infections are mild and are often never diagnosed. Serological surveys suggest that approximately 1–5% of the population in the U.S. and Europe has antibodies to LCMV. The prevalence varies with the living conditions and exposure to mice, and it has been higher in the past due to lower standards of living. The island of Vir in Croatia is one of the biggest described endemic places of origin of LCMV in the world, with IFA testing having found LCMV antibodies in 36% of the population. Individuals with the highest risk of infection are laboratory personnel who handle rodents or infected cells. Temperature and time of year is also a critical factor that contributes to the number of LCMV infections, particularly during fall and winter when mice tend to move indoors. Approximately 10–20% of the cases in immunocompetent individuals are thought to progress to neurological disease, mainly as aseptic meningitis. The overall case fatality rate is less than 1% and people with complications, including meningitis, almost always recover completely. Rare cases of meningoencephalitis have also been reported. More severe disease is likely to occur in people who are immunosuppressed.

More than 50 infants with congenital LCMV infection have been reported worldwide. The probability that a woman will become infected after being exposed to rodents, the frequency with which LCMV crosses the placenta, and the likelihood of clinical signs among these infants are still poorly understood. In one study, antibodies to LCMV were detected in 0.8% of normal infants, 2.7% of infants with neurological signs and 30% of infants with hydrocephalus. In Argentina, no congenital LCMV infections were reported among 288 healthy mothers and their infants. However, one study found that two of 95 children in a home for people with severe mental disabilities had been infected with this virus. The prognosis for severely affected infants appears to be poor. In one series, 35% of infants diagnosed with congenital infections had died by the age of 21 months.

Transplant-acquired lymphocytic choriomeningitis proves to have a very high morbidity and mortality rate. In the three clusters reported in the U.S. from 2005 to 2010, nine of the ten infected recipients died. One donor had been infected from a recently acquired pet hamster while the sources of the virus in the other cases were unknown.

Although the house mouse ("Mus musculus") is the primary reservoir host for LCMV, it is also often found in the wood mouse ("Apodemus sylvaticus") and the yellow-necked mouse ("Apodemus flavicollis"). Hamster populations can act as reservoir hosts. Other rodents including guinea pigs, rats and chinchillas can be infected but do not appear to maintain the virus. LCMV has been shown to cause illness in New World primates such as macaques, marmosets and tamarins. Infections have also been reported in rabbits, dogs and pigs. After experimental inoculation, the incubation period in adult mice is 5 to 6 days. Congenitally or neonatally infected mice and hamsters do not become symptomatic for several months or longer.

The mortality rate of the virus largely depends on the immune status of the infected dogs. Puppies experience the highest mortality rate, where complications such as pneumonia and encephalitis are more common. In older dogs that develop distemper encephalomyelitis, vestibular disease may present. Around 15% of canine inflammatory central nervous system diseases are a result of CDV.

Numerous factors have been suggested and linked to a higher risk of acquiring the infection, inclusive of malnutrition, vitamin A deficiency, absence of breastfeeding during the early stages of life, environmental pollution and overcrowding.

Mortality caused by HPIVs in developed regions of the world remains rare. Where mortality has occurred, it is principally in the three core risk groups (very young, elderly and immuno-compromised). Long term changes can however be associated with airway remodelling and are believed to be a significant cause of morbidity. The exact associations between HPIVs and diseases such as chronic obstructive pulmonary disease (COPD) are still being investigated.

In developing regions of the world, the highest risk group in terms of mortality remains pre-school children. Mortality may be as a consequence of primary viral infection or secondary problems such as bacterial infection. Predispositions, such as malnutrition and other deficiencies may further elevate the chances of mortality associated with infection.

Overall, LRI's cause approximately 25–30% of total deaths in pre-school children in the developing world. HPIVs is believed to be associated with 10% of all LRI cases, thus remaining a significant cause of mortality.

About 15–20% of hospitalized Lassa fever patients will die from the illness. The overall mortality rate is estimated to be 1%, but during epidemics, mortality can climb as high as 50%. The mortality rate is greater than 80% when it occurs in pregnant women during their third trimester; fetal death also occurs in nearly all those cases. Abortion decreases the risk of death to the mother. Some survivors experience lasting effects of the disease, and can include partial or complete deafness.

Because of treatment with ribavirin, fatality rates are continuing to decline.

MVD is caused by two viruses Marburg virus (MARV) and Ravn virus (RAVV)family Filoviridae

Marburgviruses are endemic in arid woodlands of equatorial Africa. Most marburgvirus infections were repeatedly associated with people visiting natural caves or working in mines. In 2009, the successful isolation of infectious MARV and RAVV was reported from healthy Egyptian rousettes ("Rousettus aegyptiacus") caught in caves. This isolation strongly suggests that Old World fruit bats are involved in the natural maintenance of marburgviruses and that visiting bat-infested caves is a risk factor for acquiring marburgvirus infections. Further studies are necessary to establish whether Egyptian rousettes are the actual hosts of MARV and RAVV or whether they get infected via contact with another animal and therefore serve only as intermediate hosts. Another risk factor is contact with nonhuman primates, although only one outbreak of MVD (in 1967) was due to contact with infected monkeys. Finally, a major risk factor for acquiring marburgvirus infection is occupational exposure, i.e. treating patients with MVD without proper personal protective equipment.

Contrary to Ebola virus disease (EVD), which has been associated with heavy rains after long periods of dry weather, triggering factors for spillover of marburgviruses into the human population have not yet been described.

Prognosis is generally poor. If a patient survives, recovery may be prompt and complete, or protracted with sequelae, such as orchitis, hepatitis, uveitis, parotitis, desquamation or alopecia. Importantly, MARV is known to be able to persist in some survivors and to either reactivate and cause a secondary bout of MVD or to be transmitted via sperm, causing secondary cases of infection and disease.

Of the 252 people who contracted Marburg during the 2004–2005 outbreak of a particularly virulent serotype in Angola, 227 died, for a case fatality rate of 90%.

Although all age groups are susceptible to infection, children are rarely infected. In the 1998–2000 Congo epidemic, only 8% of the cases were children less than 5 years old.

The prevalence of canine distemper in the community has decreased dramatically due to the availability of vaccinations. However, the disease continues to spread among unvaccinated populations, such as those in animal shelters and pet stores. This provides a great threat to both the rural and urban communities throughout the United States, affecting both shelter and domestic canines. Despite the effectiveness of the vaccination, outbreaks of this disease continue to occur nationally. In April 2011, the Arizona Humane Society released a valley-wide pet health alert throughout Phoenix, Arizona.

Outbreaks of canine distemper continue to occur throughout the United States and elsewhere, and are caused by many factors. These factors include the overpopulation of dogs and the irresponsibility of pet owners. The overpopulation of dogs is a national problem that organizations such as the Humane Society and ASPCA face every day. This problem is even greater within areas such as Arizona, owing to the vast amount of rural land. An unaccountable number of strays that lack vaccinations reside in these areas and are therefore more susceptible to diseases such as canine distemper. These strays act as a host for the virus, spreading it throughout the surrounding area, including urban areas. Puppies and dogs that have not received their shots can then be infected if in a place where many dogs interact, such as a dog park.

There are several diseases that are caused by avian reovirus, which includes, avian arthritis/tenosynovitis, runting-stunting syndrome, and blue wing disease in chickens. Blue wing disease affects young broiler chickens and has an average mortality rate of 10%. It causes intramuscular and subcutaneous hemorrhages and atrophy of the spleen, bursa of Fabricius, and thymus. When young chickens are experimentally infected with avian reovirus, it is spread rapidly throughout all tissues. This virus is spread most frequently in the skin and muscles, which is also the most obvious site for lesions. Avian arthritis causes significant lameness in joints, specifically the hock joints. In the most severe cases, viral arthritis has caused the tendon to rupture. Chickens that have contracted runting-stunting syndrome cause a number of individuals in a flock to appear noticeably small due to its delayed growth. Diseased chicks are typically pale, dirty, wet, and may have a distending abdomen. Some individuals may display “helicopter-like” feathers in their wings and other feather abnormalities. The virus has also been shown to cause osteoporosis.

Marburg virus is a hemorrhagic fever virus of the "Filoviridae" family of viruses and a member of the species "Marburg marburgvirus", genus "Marburgvirus". Marburg virus (MARV) causes Marburg virus disease in humans and nonhuman primates, a form of viral hemorrhagic fever. Considered to be extremely dangerous, the WHO rates it as a Risk Group 4 Pathogen (requiring biosafety level 4-equivalent containment). In the United States, the NIH/National Institute of Allergy and Infectious Diseases ranks it as a Category A Priority Pathogen and the Centers for Disease Control and Prevention lists it as a Category A Bioterrorism Agent. It is also listed as a biological agent for export control by the Australia Group.

The virus can be transmitted by exposure to one species of fruit bats or it can be transmitted between people via body fluids through unprotected copulation and broken skin. The disease can cause bleeding (haemorrhage), fever and other symptoms much like Ebola. Funeral rituals are a particular risk. Actual treatment of the virus after infection is not possible but early, professional treatment of symptoms like dehydration considerably increase survival chances.

In 2009, expanded clinical trials of an Ebola and Marburg vaccine began in Kampala, Uganda.

Fetal infection is of most consequence as this can result in the birth of a persistently infected neonate. The effects of fetal infection with BVDV are dependent upon the stage of gestation at which the dam suffers acute infection.

BVDV infection of the dam prior to conception, and during the first 18 days of gestation, results in delayed conception and an increased calving to conception interval. Once the embryo is attached, infection from days 29–41 can result in embryonic infection and resultant embryonic death.

Infection of the dam from approximately day 30 of gestation until day 120 can result in immunotolerance and the birth of calves persistently infected with the virus.

BVDV infection between 80 and 150 days of gestation may be teratogenic, with the type of birth defect dependent upon the stage of fetal development at infection. Abortion may occur at any time during gestation. Infection after approximately day 120 can result in the birth of a normal fetus which is BVD antigen-negative and BVD antibody-positive. This occurs because the fetal immune system has developed, by this stage of gestation, and has the ability to recognise and fight off the invading virus, producing anti-BVD antibodies.

BVDV infection has a wide manifestation of clinical signs including fertility issues, milk drop, pyrexia, diarrhoea and fetal infection. Occasionally, a severe acute form of BVD may occur. These outbreaks are characterized by thrombocytopenia with high morbidity and mortality. However, clinical signs are frequently mild and infection insidious, recognised only by BVDV’s immunosuppressive effects perpetuating other circulating infectious diseases (particularly scours and pneumonias).

Infection with Japanese encephalitis confers lifelong immunity. There are currently three vaccines available: SA14-14-2, IC51 (marketed in Australia and New Zealand as JESPECT and elsewhere as IXIARO) and ChimeriVax-JE (marketed as IMOJEV). All current vaccines are based on the genotype III virus.

A formalin-inactivated mouse-brain derived vaccine was first produced in Japan in the 1930s and was validated for use in Taiwan in the 1960s and in Thailand in the 1980s. The widespread use of vaccine and urbanization has led to control of the disease in Japan, Korea, Taiwan, and Singapore. The high cost of this vaccine, which is grown in live mice, means that poorer countries have not been able to afford to give it as part of a routine immunization program.

The most common adverse effects are redness and pain at the injection site. Uncommonly, an urticarial reaction can develop about four days after injection. Vaccines produced from mouse brain have a risk of autoimmune neurological complications of around 1 per million vaccinations. However where the vaccine is not produced in mouse brains but in vitro using cell culture there is little adverse effects compared to placebo, the main side effects are headache and myalgia.

The neutralizing antibody persists in the circulation for at least two to three years, and perhaps longer. The total duration of protection is unknown, but because there is no firm evidence for protection beyond three years, boosters are recommended every three years for people who remain at risk. Furthermore, there is also no data available regarding the interchangeability of other JE vaccines and IXIARO.

In September 2012 the Indian firm Biological E. Limited has launched an inactivated cell culture derived vaccine based on SA 14-14-2 strain which was developed in a technology transfer agreement with Intercell and is a thiomersal-free vaccine.

A viral disease (or viral infection) occurs when an organism's body is invaded by pathogenic viruses, and infectious virus particles (virions)

attach to and enter susceptible cells.

A vaccine has been conditionally approved for use in animals in the US. It has been shown that knockout of the NSs and NSm nonstructural proteins of this virus produces an effective vaccine in sheep as well.

Avian reoviruses belong to the genus "Orthoreovirus", and "Reoviridae" family. They are non-enveloped viruses that undergo replication in the cytoplasm of infected cells. It has icosahedral symmetry and contains a double-shelled arrangement of surface protein. Virus particles can range between 70–80 nm. Morphologically, the virus is a double stranded RNA virus that is composed of ten segments. The genome and proteins that are encoded by the genome can be separated into three different sizes ranging from small, medium, or large. Of the eleven proteins that are encoded for by the genome, two are nonstructural, while the remaining nine are structural.

Avian reoviruses can withstand a pH range of 3.0–9.0. Ambient temperatures are suitable for the survival of these viruses, which become inactive at 56 °C in less than an hour. Common areas where this virus can survive include galvanized metal, glass, rubber, feathers, and wood shavings. Avian reovirus can survive for up to ten days on these common areas in addition to up to ten weeks in water.

Cultivation and observation of the effects of avian reovirus is most often performed in chicken embryos. If infected into the yolk sac, the embryo will succumb to death accompanied by hemorrhaging of the embryos and cause the foci on the liver to appear yellowish-green. There are several primary chicken cell cultures/areas that are susceptible to avian reoviruses, which include the lungs, liver, kidney, and fibroblasts of the chick embryo. Of the following susceptible areas, liver cells from the chick embryo have been found to be the most sensitive for primary isolation from clinical material.

Typically, the CPE effect of avian reoviruses is the production of syncytia. CPE, or cytopathic effects are the visible changes in a host cell that takes place because of viral infection. Syncytia is a single cell or cytoplasmic mass containing several nuclei, formed by fusion of cells or by division of nuclei.

The number of people infected by Lassa range from 100,000 to three million a year, with up to 5,000 deaths per year in West Africa alone. In certain areas such as Sierra Leone and Liberia, 10-16% of people admitted to hospital have the virus. The case fatality rate for those who are hospitalized for the disease is about 15-20%. Research in Guinea showed a twofold increase risk of infection for those living in close proximity to someone with infection symptoms within the last year.

Lassa has been linked to high risk areas near the western and eastern extremes of West Africa. These areas cannot be well defined by any known biogeographical or environmental breaks. However, it is relatively common in parts of West Africa where the multimammate rat is common, particularly Guinea (Kindia, Faranah and Nzerekore regions), Liberia (mostly in Lofa, Bong, and Nimba counties), Nigeria (everywhere) and Sierra Leone (typically from Kenema and Kailahun districts). It is present but less common in the Central African Republic, Mali, Senegal and other nearby countries, and less common yet in Ghana and the Democratic Republic of the Congo. Benin had its first confirmed cases in 2014, and Togo had its first confirmed cases in 2016.

The spread of Lassa outside of West Africa has been very limited. Twenty to thirty cases have been described in Europe, cited as being caused by importation through infected individuals. These causes found outside of West Africa were found to have a high fatality risk because of the delay of diagnosis and treatment due to being unaware of the risk associated with the symptoms. These imported cases have not manifested in larger epidemics outside of Africa due to a lack of human to human transmission in hospital settings. The exception of this happened in 2003 when a healthcare worker became infected before the patient showed clear symptoms.

The study of the epidemiology of Lassa fever is complicated by a lengthy incubation period, which may be up to three weeks. Incubation periods as long as Lassa fever may affect spatial clustering of the disease by limiting the understanding of the incidence and distribution of the disease. The spatial clustering for this disease is still in development as a lack of easy-available diagnosis, limited public health surveillance infrastructure, and high clustering of incidence near high intensity sampling make for an incomplete look at the impact of Lassa in this region.

One study has focused on identifying OROV through the use of RNA extraction from reverse transcription-polymerase chain reaction. This study revealed that OROV caused central nervous system infections in three patients. The three patients all had meningoencephalitis and also showed signs of clear lympho-monocytic cellular pattern in CSF, high protein, and normal to slightly decreased glucose levels indicating they had viral infections. Two of the patients already had underlying infections that can effect the CNS and immune system and in particular one of these patients has HIV/AIDS and the third patient has neurocysticercosis. Two patients were infected with OROV developed meningitis and it was theorized that this is due to them being immunocompromised. Through this it was revealed that it's possible that the invasion of the central nervous system by the oropouche virus can be performed by a pervious blood-brain barrier damage.

Prophylaxis by vaccination, as well as preventive measures like protective clothing, tick control, and mosquito control are advised. The vaccine for KFDV consists of formalin-inactivated KFDV. The vaccine has a 62.4% effectiveness rate for individuals who receive two doses. For individuals who receive an additional dose, the effectiveness increases to 82.9%. Specific treatments are not available.

Prevention strategies include reducing the breeding of midges through source reduction (removal and modification of breeding sites) and reducing contact between midges and people. This can be accomplished by reducing the number of natural and artificial water-filled habitats and encourage the midge larvae to grow.

Oropouche fever is present in epidemics so the chances of one contracting it after being exposed to areas of midgets or mosquitoes is rare.

Symptoms of infectious mononucleosis are fever, sore throat, and swollen lymph glands. Sometimes, a swollen spleen or liver involvement may develop. Heart problems or involvement of the central nervous system occurs only rarely, and infectious mononucleosis is almost never fatal. There are no known associations between active EBV infection and problems during pregnancy, such as miscarriages or birth defects. Although the symptoms of infectious mononucleosis usually resolve in 1 or 2 months, EBV remains dormant or latent in a few cells in the throat and blood for the rest of the person's life. Periodically, the virus can reactivate and is commonly found in the saliva of infected persons. Reactivated and post-latent virus may pass the placental barrier in (also seropositive) pregnant women via macrophages and therefore can infect the fetus. Also re-infection of prior seropositive individuals may occur. In contrast, reactivation in adults usually occurs without symptoms of illness.

EBV also establishes a lifelong dormant infection in some cells of the body's immune system. A late event in a very few carriers of this virus is the emergence of Burkitt's lymphoma and nasopharyngeal carcinoma, two rare cancers. EBV appears to play an important role in these malignancies, but is probably not the sole cause of disease.

Most individuals exposed to people with infectious mononucleosis have previously been infected with EBV and are not at risk for infectious mononucleosis. In addition, transmission of EBV requires intimate contact with the saliva (found in the mouth) of an infected person. Transmission of this virus through the air or blood does not normally occur. The incubation period, or the time from infection to appearance of symptoms, ranges from 4 to 6 weeks. Persons with infectious mononucleosis may be able to spread the infection to others for a period of weeks. However, no special precautions or isolation procedures are recommended, since the virus is also found frequently in the saliva of healthy people. In fact, many healthy people can carry and spread the virus intermittently for life. These people are usually the primary reservoir for person-to-person transmission. For this reason, transmission of the virus is almost impossible to prevent.

The clinical diagnosis of infectious mononucleosis is suggested on the basis of the symptoms of fever, sore throat, swollen lymph glands, and the age of the patient. Usually, laboratory tests are needed for confirmation. Serologic results for persons with infectious mononucleosis include an elevated white blood cell count, an increased percentage of certain atypical white blood cells, and a positive reaction to a "mono spot" test.

The U.S. Centers for Disease Control and Prevention (CDC) publishes a journal "Emerging Infectious Diseases" that identifies the following factors contributing to disease emergence:

- Microbial adaption; e.g. genetic drift and genetic shift in Influenza A

- Changing human susceptibility; e.g. mass immunocompromisation with HIV/AIDS

- Climate and weather; e.g. diseases with zoonotic vectors such as West Nile Disease (transmitted by mosquitoes) are moving further from the tropics as the climate warms

- Change in human demographics and trade; e.g. rapid travel enabled SARS to rapidly propagate around the globe

- Economic development; e.g. use of antibiotics to increase meat yield of farmed cows leads to antibiotic resistance

- Breakdown of public health; e.g. the current situation in Zimbabwe

- Poverty and social inequality; e.g. tuberculosis is primarily a problem in low-income areas

- War and famine

- Bioterrorism; e.g. 2001 Anthrax attacks

- Dam and irrigation system construction; e.g. malaria and other mosquito borne diseases

Viral disease is usually detected by clinical presentation, for instance severe muscle and joint pains preceding fever, or skin rash and swollen lymph glands.

Laboratory investigation is not directly effective in detecting viral infections, because they do not themselves increase the white blood cell count. Laboratory investigation may be useful in diagnosing associated bacterial infections, however.

Viral infections are commonly of limited duration, so treatment usually consists in reducing the symptoms; antipyretic and analgesic drugs are commonly prescribed.

West Nile virus (WNV) is a single-stranded RNA virus that causes West Nile fever. It is a member of the family Flaviviridae, specifically from the genus Flavivirus which also contain the Zika virus, dengue virus, and the yellow fever virus. The West Nile virus is primarily transmitted through mosquitoes, mostly by the Culex species. However, ticks have been found to carry the virus. The primary hosts of WNV are birds, so that the virus remains within a "bird-mosquito-bird" transmission cycle.