There are three main viruses that have been studied and confirmed as the agents responsible for AHC, including enterovirus 70, coxsakievirus A24 variant (CA24v) and adenovirus 11.

AHC can only exist in a human host and is transmitted through human contact with an infected individual or object, such as a towel used by an infected person. It is also easily communicable through fecal-oral pathways, thus allowing for its abundance in areas of the world with low levels of hygiene. Within one to two days of infection, symptoms will begin to become apparent.

Enterovirus 70 is a member of the genus of viruses called Enterovirus and family of the viruses Picornaviridae. Usually very small (about 30 nm in diameter), it is non-enveloped (meaning it only has a nucleic acid core and protein capsid) and has a single-stranded positive-sense RNA genome; the protein capsid the virus itself is surrounded by is icosahedral. It is known as one of the more new enteroviruses within this category. It spreads easily from one person’s eyes to another’s through contact with infected objects, like fingers, or through the eye secretion itself. Enterovirus 70 infrequently causes polio-like permanent paralysis.

The risk factors associated with BPF are not well known. However, it has been suggested that children under 5 years of age are more susceptible to BPF since they lack serum bactericidal activity against the infection. Older children and adults have much higher titers of bactericidal antibodies, which serve as a protective measure. Also children residing in warmer geographic areas have been associated with a higher risk of BPF infection.

Most household disinfectants will inactivate FHV-1. The virus can survive up to 18 hours in a damp environment, but less in a dry environment and only shortly as an aerosol.

FVR is transmitted through direct contact only. It replicates in the nasal and nasopharyngeal tissues and the tonsils. Viremia (the presence of the virus in the blood) is rare. The virus is shed in saliva and eye and nasal secretions, and can also be spread by fomites. FVR has a two- to five-day incubation period. The virus is shed for one to three weeks postinfection. Latently infected cats (carriers) will shed FHV-1 intermittently for life, with the virus persisting within the trigeminal ganglion. Stress and use of corticosteroids precipitate shedding. Most disinfectants, antiseptics and detergents are effective against the virus.

Although epidemiologic characteristics of the adenoviruses vary by type, all are transmitted by direct contact, fecal-oral transmission, and occasionally waterborne transmission. Some types are capable of establishing persistent asymptomatic infections in tonsils, adenoids, and intestines of infected hosts, and shedding can occur for months or years. Some adenoviruses (e.g., serotypes 1, 2, 5, and 6) have been shown to be endemic in parts of the world where they have been studied, and infection is usually acquired during childhood. Other types cause sporadic infection and occasional outbreaks; for example, epidemic keratoconjunctivitis is associated with adenovirus serotypes 8, 19, and 37. Epidemics of febrile disease with conjunctivitis are associated with waterborne transmission of some adenovirus types, often centering on inadequately chlorinated swimming pools and small lakes. ARD is most often associated with adenovirus types 4 and 7 in the United States. Enteric adenoviruses 40 and 41 cause gastroenteritis, usually in children. For some adenovirus serotypes, the clinical spectrum of disease associated with infection varies depending on the site of infection; for example, infection with adenovirus 7 acquired by inhalation is associated with severe lower respiratory tract disease, whereas oral transmission of the virus typically causes no or mild disease. Outbreaks of adenovirus-associated respiratory disease have been more common in the late winter, spring, and early summer; however, adenovirus infections can occur throughout the year.

"Ad14 (for adenovirus serotype 14), has caused at least 140 illnesses in New York, Oregon, Texas and Washington, according to a report from the Centers for Disease Control and Prevention. The illness made headlines in Texas in September 2007, when a so-called "boot camp flu" sickened hundreds at Lackland Air Force Base in San Antonio. A 19-year-old trainee died."

Several adenoviruses, including Ad5, Ad9, Ad31, Ad36, Ad37, and SMAM1, have at least some evidence of causation of obesity in animals, adipogenesis in cells, and/or association with human obesity. To date, the most thorough investigations have been conducted for adenovirus serotype 36 (Adv36).

Adenovirus can cause severe necrotizing pneumonia in which all or part of a lung has increased translucency radiographically, which is called Swyer-James Syndrome. Severe adenovirus pneumonia also may result in bronchiolitis obliterans, a subacute inflammatory process in which the small airways are replaced by scar tissue, resulting in a reduction in lung volume and lung compliance.

A vaccine is available in the UK and Europe, however in laboratory tests it is not possible to distinguish between antibodies produced as a result of vaccination and those produced in response to infection with the virus. Management also plays an important part in the prevention of EVA.

Many viral infections of the central nervous system occur in seasonal peaks or as epidemics, whereas others, such as herpes simplex encephalitis, are sporadic. In endemic areas it is mostly a disease of children, but as the disease spreads to new regions, or nonimmune travelers visit endemic regions, nonimmune adults are also affected.

Meningitis is a very common in children. Newborns can develop herpes virus infections through contact with infected secretions in the birth canal. Other viral infections are acquired by breathing air contaminated with virus-containing droplets exhaled by an infected person. Arbovirus infections are acquired from bites by infected insects (called epidemic encephalitis). Viral central nervous system infections in newborns and infants usually begin with fever. The inability of infants to communicate directly makes it difficult to understand their symptoms. Newborns may have no other symptoms and may initially not otherwise appear ill. Infants older than a month or so typically become irritable and fussy and refuse to eat. Vomiting is common. Sometimes the soft spot on top of a newborn's head (fontanelle) bulges, indicating an increase in pressure on the brain. Because irritation of the meninges is worsened by movement, an infant with meningitis may cry more, rather than calm down, when picked up and rocked. Some infants develop a strange, high-pitched cry. Infants with encephalitis often have seizures or other abnormal movements. Infants with severe encephalitis may become lethargic and comatose and then die. To make the diagnosis of meningitis or the diagnosis of encephalitis, doctors do a spinal tap (lumbar puncture) to obtain cerebrospinal fluid (CSF) for laboratory analysis in children.

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.

The mortality rate of chikungunya is slightly less than 1 in 1000. Those over the age of 65, neonates, and those with underlying chronic medical problems are most likely to have severe complications. Neonates are vulnerable as it is possible to vertically transmit chikungunya from mother to infant during delivery, which results in high rates of morbidity, as infants lack fully developed immune systems. The likelihood of prolonged symptoms or chronic joint pain is increased with increased age and prior rheumatological disease.

The best prevention against viral pneumonia is vaccination against influenza, adenovirus, chickenpox, herpes zoster, measles, and rubella.

The eye gnat ("Liohippelates") was thought to be the cause of the conjunctivitis epidemic which occurred in Mato Grosso do Sul in 1991. These gnats were extracted from the conjunctival secretions of the children who were infected with conjunctivitis. 19 of those children developed BPF following the conjunctivitis. Other modes of transmission include contact with the conjunctival discharges of infected people, ophthalmic instruments which have not been properly sterilized, sharing eye makeup applicators or multiple-dose eye medications.

EVA is caused by an arterivirus called equine arteritis virus (EAV). Arteriviruses are small, enveloped, animal viruses with an icosahedral core containing a positive-sense RNA genome. As well as equine arteritis virus the Arterivirus family includes porcine reproductive and respiratory syndrome virus (PRRSV), lactate dehydrogenase elevating virus (LDV) of mice and simian haemorrhagic fever virus (SHFV).

There are a number of routes of transmission of the virus. The most frequent is the respiratory route. The virus can also be spread by the venereal route, including by artificial insemination. Stallions may become carriers.

Dogs will typically recover from kennel cough within a few weeks. However, secondary infections could lead to complications that could do more harm than the disease itself. Several opportunistic invaders have been recovered from the respiratory tracts of dogs with kennel cough, including Streptococcus, Pasteurella, Pseudomonas, and various coliforms. These bacteria have the potential to cause pneumonia or sepsis, which drastically increase the severity of the disease. These complications are evident in thoracic radiographic examinations. Findings will be mild in animals affected only by kennel cough, while those with complications may have evidence of segmental atelectasis and other severe side effects.

Lassa virus is a member of the Arenavirida family of viruses. Specifically it is an old world arenavirus, which is enveloped, single-stranded, and bi-segmented RNA. This virus has a both a large and a small genome section, with four lineages identified to date: Josiah (Sierra Leone), GA391 (Nigeria), LP (Nigeria) and strain AV.

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.

Observations during recent epidemics have suggested chikungunya may cause long-term symptoms following acute infection. This condition has been termed chronic chikungunya virus-induced arthralgia. Long-term symptoms are not an entirely new observation; long-term arthritis was observed following an outbreak in 1979. Common predictors of prolonged symptoms are advanced age and prior rheumatological disease.

During the La Reunion outbreak in 2006, more than 50% of subjects over the age of 45 reported long-term musculoskeletal pain with up to 60% of people reporting prolonged painful joints three years following initial infection. A study of imported cases in France reported that 59% of people still suffered from arthralgia two years after acute infection. Following a local epidemic of chikungunya in Italy, 66% of people reported muscle pains, joint pains, or asthenia at one year after acute infection.

Currently, the cause of these chronic symptoms is not fully known. Markers of autoimmune or rheumatoid disease have not been found in people reporting chronic symptoms. However, some evidence from humans and animal models suggests chikungunya may be able to establish chronic infections within the host. Viral antigen was detected in a muscle biopsy of a person suffering a recurrent episode of disease three months after initial onset. Additionally, viral antigen and viral RNA were found in macrophages in the synovial joint of a person experiencing a relapse of musculoskeletal disease 18 months after initial infection. Several animal models have also suggested chikungunya virus may establish persistent infections. In a mouse model, viral RNA was detected specifically in joint-associated tissue for at least 16 weeks after inoculation, and was associated with chronic synovitis. Similarly, another study reported detection of a viral reporter gene in joint tissue of mice for weeks after inoculation. In a nonhuman primate model, chikungunya virus was found to persist in the spleen for at least six weeks.

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.

The most common causes of viral meningitis in the United States are non-polio enteroviruses. The viruses that cause meningitis are typically acquired from sick contacts. However, in most cases, people infected with viruses that may cause meningitis do not actually develop meningitis.

Viruses that can cause meningitis include:

Viral infections such as canine parainfluenza or canine coronavirus are only shed for roughly 1 week following recovery; however, respiratory infections involving "Bordetella bronchiseptica" can be transmissible for several weeks longer. While there was early evidence to suggest that "B. bronchiseptica" could be shed for many months post-infection, a more recent report places detectable nasal and pharyngeal levels of "B. bronchiseptica" in 45.6% of all clinically healthy dogs. This has potentially expanded the vector from currently or recently infected dogs to half the dog population as carriers. To put the relative levels of shedding bacteria into perspective, a study analyzing the shedding kinetics of "B. bronchiseptica" presents the highest levels of bacterial shedding one week post-exposure, with an order of magnitude decrease in shedding observed every week. This projection places negligible levels of shedding to be expected 6 weeks post-exposure (or ~5 weeks post-onset of symptoms). Dogs which had been administered intranasal vaccine 4 weeks prior to virulent "B. bronchiseptica" challenge displayed little to no bacterial shedding within 3 weeks of exposure to the virulent strain.

Viral entry is the earliest stage of infection in the viral life cycle, as the virus comes into contact with the host cell and introduces viral material into the cell. The major steps involved in viral entry are shown below. Despite the variation among viruses, there are several shared generalities concerning viral entry.

From 1988–1999, about 36,000 cases occurred each year. While the disease can occur in both children and adults, it is more common in children. During an outbreak in Romania and in Spain viral meningitis was more common among adults. While, people aged younger than 15 made up 33.8% of cases. In contrast in Finland in 1966 and in Cyprus in 1996, Gaza 1997, China 1998 and Taiwan 1998, the incidences of viral meningitis were more common among children.

The majority of people survive measles, though in some cases, complications may occur. Possible consequences of measles virus infection include bronchitis, sensorineural hearing loss, and—in about 1 in 10,000 to 1 in 300,000 cases—panencephalitis, which is usually fatal. Acute measles encephalitis is another serious risk of measles virus infection. It typically occurs two days to one week after the breakout of the measles rash and begins with very high fever, severe headache, convulsions and altered mentation. A person with measles encephalitis may become comatose, and death or brain injury may occur.