All the diseases caused by viruses

Antivirals should be distinguished from viricides, which are usually used a disinfectants rather than medications, but deactivate or destroy virus particles, either inside or outside the body.

A very early stage of viral infection is viral entry, when the virus attaches to and enters the host cell. Inhibitors of uncoating have also been investigated.

Amantadine and rimantadine have been introduced to combat influenza. These agents act on this penetration and uncoating process. Pleconaril works against rhinoviruses, which cause the common cold, by blocking a pocket on the surface of the virus that controls the uncoating process.

This pocket is similar in most strains of rhinoviruses and enteroviruses, which can cause diarrhea, meningitis, conjunctivitis, and encephalitis. The problem today with antibiotics or antibacterials, antifungicides, and antiviruses is resistance. Antimicrobial resistance is resistance of a microorganism to an antimicrobial drug that was originally effective for treatment of infections caused by it.

Resistant microorganisms bacteria, fungi, viruses, and parasites are able to withstand attack by antimicrobial drugs so that standard treatments become ineffective and infections persist, increasing the risk of spread to others. The evolution of resistant strains is a natural phenomenon that occurs when microorganisms replicate themselves erroneously or when resistant traits are exchanged between them. When resistance occurs it is necessary to form modified drugs to avoid resistance.

For instance, ampicillin and amoxicillin are variants of penicillin to work around resistance of common infections.

Know these keywords and what each word refers to as well as its function. Read over the list. Are all these keywords familiar? Answer these questions. Do you know the answers, holy cow! Check yourself out in this quiz, and prove that you are a humanology wiz. Try out PMC Labs and tell us what you think. Learn More. There are virus species that are known to be able to infect humans. The first of these to be discovered was yellow fever virus in , and three to four new species are still being found every year.

Extrapolation of the discovery curve suggests that there is still a substantial pool of undiscovered human virus species, although an apparent slow-down in the rate of discovery of species from different families may indicate bounds to the potential range of diversity.

More than two-thirds of human viruses can also infect non-human hosts, mainly mammals, and sometimes birds. Many specialist human viruses also have mammalian or avian origins. Indeed, a substantial proportion of mammalian viruses may be capable of crossing the species barrier into humans, although only around half of these are capable of being transmitted by humans and around half again of transmitting well enough to cause major outbreaks.

A few possible predictors of species jumps can be identified, including the use of phylogenetically conserved cell receptors. It seems almost inevitable that new human viruses will continue to emerge, mainly from other mammals and birds, for the foreseeable future. For this reason, an effective global surveillance system for novel viruses is needed. New species of human virus are still being identified, at a rate of three or four per year see below , and viruses make up over two-thirds of all new human pathogens [ 2 ], a highly significant over-representation given that most human pathogen species are bacteria, fungi or helminths.

These new viruses differ wildly in their importance, ranging from the rare and mild illness due to Menangle virus to the devastating public health impact of HIV In this paper, we take an ecological approach to studying the diversity of human viruses defined as viruses for which there is evidence of natural infection of humans.

As experiences with HIV-1 and new variants of influenza A and also with novel animal pathogens such as canine parvovirus [ 4 ] show, this shift can occur rapidly, over time scales of decades, years or even months.

Indeed, the demarcation between genus, species complex, species and serotype or other designations of sub-specific variation can be somewhat arbitrary.

As a starting point for our survey, we used a previously published database see [ 5 ] obtained by systematically searching the primary scientific literature up to and including for reports of human infection with recognized virus species, using species as defined by the International Committee on Taxonomy of Viruses ICTV [ 6 ]. The list of viruses was updated if either a new species that can infect humans had been described in the literature and also recognized by the ICTV, if a known species had been found in humans for the first time, or if there had been a change in species classifications by the ICTV notably for the human papillomaviruses and the vesicular stomatitis viruses.

The year of discovery was taken to be the year of publication of the first report of human infection. The place of discovery was determined from the original report and recorded as the location of the diagnostic laboratory or, in the few instances where this was not clear, the address of the first author of the report.

We did not attempt to locate the case itself, as this information was often lacking. We obtained a list of ICTV-recognized virus species that have been reported to infect humans.

The discovery curve is an ecological tool for estimating species diversity [ 7 ] comprising a simple plot of the cumulative number of species against time or sampling effort. The discovery curve for human virus species is shown in figure 1 a. Discovery curves for human viruses. Cumulative number of species reported to infect humans. Statistically significant upward breakpoints are shown vertical lines. Cumulative number of families containing species reported to infect humans.

Major developments in the technology of virus discovery adapted from [ 8 ]. Since the mean rate of discovery has been 3. However, there has been a slight but statistically significant downward trend in the rate of discovery a linear regression of count per year 0.

Numbers of species discovered by continent are shown in figure 2 a ignoring four species for which the location of discovery could not be determined. That over 60 per cent of species were first discovered in North America or Europe almost certainly reflects considerable ascertainment bias [ 9 , 10 ].

Rates of discovery by continent have, perhaps unsurprisingly, been very variable through time but with no clear patterns; the only notable trend in the last 15 years has been a higher rate of discovery in Australasia. Patterns in human virus diversity. Twenty three families are represented; six virus species remain unassigned to a family. Numbers of species by family are shown in figure 2 b. The family containing the most human virus species is the Bunyaviridae with 40; six families contain just one human virus species.

These numbers are too small for statistical analysis of rates of discovery: the most notable trend is that only a single new pox virus has been discovered since compared with 10 up to that date. Following the approach described previously [ 5 ], we modelled human virus discovery since , assuming a total number of species available to be discovered—the species pool—of N virus species, each discovered in any given year with probability p.

We considered fitting a distribution for values of p ; however, provided that the individual p values are low, there was minimal improvement in model fit. The model was fitted to the data and evaluated using Markov chain Monte Carlo MCMC methods with flat prior information to calculate profile likelihood confidence intervals and the best fit parameters.

However, the binomial distribution B N , p can be accurately approximated by a Poisson distribution with parameter Np for the range of values of N and p of interest. We compared the model with the observed data by calculating the mean, trend in the mean and variance for the number of virus species discovered per year based on 5 million simulations using best fit parameter values. The model reproduces the observed data well: observed mean and variance 3. Parameter estimates, however, are very uncertain owing to an unavoidable strong correlation between N and p [ 5 ].

The estimate of N is of particular interest: this has a central value of i. Thus, although there is considerable uncertainty as to the size of the human virus species pool, this analysis suggests that there are at least dozens of new species to be discovered, and possibly a very much larger number. This projection, of course, makes no allowance for any improvements in virus detection technology nor changes in discovery effort.

From our systematic literature review, we identified at least 14 putative new species of human virus first reported during the 5 years to inclusive table 2 , though this list is almost certainly incomplete.

Indeed, it would be unsurprising if it were exceeded, given the considerable recent interest in virus discovery and the advent of high throughput sequencing as a detection tool. Examples of putative new human virus species reported from to [ 11 — 24 ]. The discovery curve for virus families is shown in figure 1 b. Here, a family is included on the date of the first published report of human infection by a virus species from that family. Strikingly, no new families have been added to the list since , the longest such interval on record.

It should also be noted that there are three virus families that, although they do not contain any known human virus species, do contain species that infect other mammals: Arteriviridae several species including simian haemorrhagic fever virus ; Asfarviridae African swine fever virus ; Circoviridae including mammal infecting circoviruses as well as gyrovirus which infects chickens.

This suggests that the list of families containing human viruses may not yet be complete. More than two-thirds of human virus species are zoonotic, i. By far the most important non-human host taxa are other mammals, with rodents and ungulates most commonly identified as alternative hosts, followed by primates, carnivores and bats.

In some cases, the antiviral drug ribavirin may be given. Researchers are in the process of developing vaccines for several hemorrhagic viruses. A yellow fever vaccine is currently available for people traveling to areas where yellow fever is common. If you live or work in an area where viral hemorrhagic diseases are common, you can do the following to reduce your risk:.

Some viruses can infect the brain and surrounding tissues, causing neurologic viral diseases. This can result in a range of symptoms, including:. Many neurologic viruses are spread through the bite of an infected animal or bug, such as a mosquito or tick. Other viruses, such poliovirus and other enteroviruses, are quite contagious and spread through close contact with someone with the virus.

Contaminated objects can also contribute to the spread of these viruses. Getting plenty of rest, staying hydrated, and taking OTC anti-inflammatories to ease pain or headaches can all help. In some cases, antiviral medication may be prescribed. Polio or severe cases of meningitis or encephalitis may require additional treatment, such as breathing assistance or IV fluids.

Practicing good hygiene, avoiding close contact with those who have the virus, and protecting against insect bites can all help to reduce the spread of encephalitis and meningitis. To reduce the risk of spreading rabies, keep your pets vaccinated and avoid approaching wild animals.

There are many viral diseases. Some, such as the common cold or the stomach flu, are minor and go away on their own within a few days. Others, however, are more serious. Instead, treatment usually focuses on managing symptoms and supporting the immune system with plenty of rest and hydration.

Post-viral fatigue is a type of extreme tiredness that sometimes happens after a recent viral infection. We'll go over its common symptoms, how it's…. A viral fever is an uncomfortable symptom of many viral illnesses. Viral rashes can affect children and adults alike. Learn how to recognize them, the viruses that cause them, and how they're spread, treated, and more.

A viral fever is a high body temperature that accompanies many viral infections. Find out how they compare to flu or hay fever, emergency symptoms, and…. The risk of getting a false positive result for COVID is relatively low but false negatives are common. Viral shedding occurs from lesions but can occur even when lesions are not apparent. After the initial infection, HSV remains dormant in nerve ganglia, from which it can periodically emerge, causing symptoms.

Recurrent herpetic eruptions are precipitated by. After initial infection, all herpesviruses remain latent within specific host cells and may subsequently Mucocutaneous infection most common , including genital herpes Genital Herpes Genital herpes is a sexually transmitted disease caused by human herpesvirus 1 or 2. It causes ulcerative genital lesions. Diagnosis is clinical with laboratory confirmation by culture, polymerase Ocular infection including herpes keratitis Herpes Simplex Keratitis Herpes simplex keratitis is corneal infection with herpes simplex virus.

It may involve the iris. Symptoms and signs include foreign body sensation, lacrimation, photophobia, and conjunctival A typical sign is vesicular eruption, which may be accompanied by or progress to disseminated disease. Progressive and persistent esophagitis, colitis, perianal ulcers, pneumonia, encephalitis, and meningitis may occur.

HSV outbreaks may be followed by erythema multiforme Erythema Multiforme Erythema multiforme is an inflammatory reaction, characterized by target or iris skin lesions.

Oral mucosa may be involved. Diagnosis is clinical. Lesions spontaneously resolve but frequently Eczema herpeticum Complications Atopic dermatitis is a chronic relapsing inflammatory skin disorder with a complex pathogenesis involving genetic susceptibility, immunologic and epidermal barrier dysfunction, and environmental Lesions may appear anywhere on the skin or mucosa but are most frequent in the following locations:.

Generally, after a prodromal period typically Vesicles typically persist for a few days, then rupture and dry, forming a thin, yellowish crust. Healing generally occurs within 10 to 19 days after onset in primary infection or within 5 to 10 days in recurrent infection. Lesions usually heal completely, but recurrent lesions at the same site may cause atrophy and scarring. Skin lesions can develop secondary bacterial infection. In patients with depressed cell-mediated immunity due to HIV infection or other conditions, prolonged or progressive lesions may persist for weeks or longer.

Localized infections can disseminate, particularly—and often dramatically—in immunocompromised patients. Acute herpetic gingivostomatitis usually results from primary infection with HSV-1, typically in children.

Herpetic pharyngitis can occur in adults as well as children. Occasionally, through oral-genital contact, the cause is HSV Intraoral and gingival vesicles rupture, usually within several hours to 1 or 2 days, to form ulcers. Fever and pain often occur. Difficulty eating and drinking may lead to dehydration. After resolution, the virus resides dormant in the semilunar ganglion.