Question: Are all types of cellular life infected by it?
About the article "Virus", section "Host range".

Candidate passages:
Viruses infect all cellular life and, although viruses occur universally, each cellular species has its own specific range that often infect only that species.
Some viruses, called satellites, can replicate only within cells that have already been infected by another virus. 
A well-known classification of cellular automata by Stephen Wolfram studies their behavior on random initial conditions.
For a reversible cellular automaton, if the initial configuration is chosen uniformly at random among all possible configurations, then that same uniform randomness continues to hold for all subsequent states.
Thus it would appear that most reversible cellular automata are of Wolfram's Class 3: automata in which almost all initial configurations evolve pseudo-randomly or chaotically.
However, it is still possible to distinguish among different reversible cellular automata by analyzing the effect of local perturbations on the behavior of the automaton: making a change to the initial state of a reversible cellular automaton may cause changes to later states to remain only within a bounded region, to propagate irregularly but unboundedly, or to spread quickly, and lists one-dimensional reversible cellular automaton rules exhibiting all three of these types of behavior.
Later work by Wolfram identifies the one-dimensional Rule 37R automaton as being particularly interesting in this respect: when run with a small seed of random cells centered within a larger neighborhood, with a finite number of cells with circular boundary conditions, it tends to fluctuate between ordered and chaotic states, while with the same initial conditions on an unbounded set of cells its configurations tend to organize themselves into several types of simple moving particles. 
People with the advanced HIV often exhibit psoriasis.
The prevalence of psoriasis in HIV-positive individuals is comparable to that of HIV-negative individuals, however, psoriasis tends to be more severe in people infected with HIV.
There is a much higher prevalence of psoriatic arthritis in HIV-positive individuals with psoriasis than in those without the infection.
The immune response in those infected with HIV is typically characterized by cellular signals from Th2 subset of CD4+ helper T cells, whereas the immune response in psoriasis vulgaris is characterized by a pattern of cellular signals typical of Th1 subset of CD4+ helper T cells and Th17 helper T cells.
It is hypothesized that the diminished CD4+-T cell presence causes an overactivation of CD8+-T cells, which are responsible for the exacerbation of psoriasis in HIV-positive people.
Psoriasis in those with HIV/AIDS is often severe and may be untreatable with conventional therapy.
People with HIV constitute 1% of all people with psoriasis. 
Neither macroscopic nor microscopic lesions have been reported for nonpregnant pigs.
It is conceivable that cellular infiltrations subsequently described for fetuses could be induced by infection during the perinatal interval.
Macroscopic lesions have not been reported in pregnant dams; however, microscopic lesions have been seen in tissues of gilts killed after their fetuses were infected by transuterine inoculation of virus.
Gilts that were seronegative when their fetuses were infected at 70 days of gestation had focal accumulations of mononuclear cells adjacent to the endometrium and in deeper layers of the lamina propria when they were killed 12 and 21 days later.
In addition, there were perivascular cuffs of plasma cells and lymphocytes in the brain, spinal cord, and choroid of the eye.
When fetuses were infected earlier in gestation (35, 50, and 60 days) and their dams were killed 7 and 11 days later, the lesions were similar.
However, uterine lesions were more severe and also included extensive cuffing of myometrial and endometrial vessels with mononuclear cells.
Only focal accumulations of lymphocytes were seen in uteruses of gilts that were seropositive when their fetuses were infected.
Macroscopic changes of embryos are death followed by resorption of fluids (Fig.
4) and then soft tissues (Fig.
5).
Virus and viral antigen are widely distributed in tissues of infected embryos and their placentas, and it is probable that microscopic lesions of necrosis and vascular damage, subsequently described for fetuses, also develop in advanced embryos.
There are numerous macroscopic changes in fetuses infected before they become immunocompetent (Fig.
6).
These include a variable degree of stunting and sometimes an obvious loss of condition before other external changes are apparent; occasionally, an increased prominence of blood vessels over the surface of the fetus due to congestion and leakage of blood into contiguous tissues; congestion, edema, and hemorrhage with accumulation of serosanguineous fluids in body cavities; hemorrhagic discoloration becoming progressively darker after death; and dehydration (mummification).
Many of these changes also apply to the placenta.
Microscopic lesions consist primarily of extensive cellular necrosis in a wide variety of tissues and organs (Fig.
7A).
Inflammation and intranuclear inclusions also have been described.
In contrast, macroscopic changes have not been reported for fetuses infected after they become immunocompetent for PPV.
Microscopic lesions are primarily endothelial hypertrophy and mononuclear cell infiltrations consistent with an immune response.
Meningoencephalitis characterized by perivascular cuffing with proliferating adventitial cells, histiocytes, and a few plasma cells was seen in the gray and white matter of the cerebrum and in the leptomeninges of PPV-infected stillborn pigs.
These lesions were believed to be pathognomonic for PPV infection.
Similar lesions have been observed in PPV-infected, live fetuses collected late in gestation (Fig.
Both general types of microscopic lesions (i.e., necrosis and mononuclear cell infiltration) may develop in fetuses infected near midgestation when the immune response is insufficient to provide protection. 
Over 100 different HPV types have been identified and are referred to by number.
About a dozen HPV types, including types 16, 18, 31 and 45, are called "high-risk" types because they can lead to cervical cancer, as well as anal cancer, vulvar cancer, and penile cancer.
Several types of HPV, particularly type 16, have been found to be associated with oropharyngeal squamous-cell carcinoma, a form of head and neck cancer.
HPV-induced cancers often have viral sequences integrated into the cellular DNA.
Some of the HPV "early" genes, such as E6 and E7, are known to act as oncogenes that promote tumor growth and malignant transformation.
An infection with one or more high-risk HPV types is believed to be a prerequisite for the development of cervical cancer (the vast majority of HPV infections are not high risk); according to the American Cancer Society, women with no history of the virus do not develop this type of cancer.
However, most HPV infections are cleared rapidly by the immune system and do not progress to cervical cancer.
Because the process of transforming normal cervical cells into cancerous ones is slow, cancer occurs in people who have been infected with HPV for a long time, usually over a decade or more.HPV infection is a necessary factor in the development of nearly all cases of cervical cancer.
A cervical Pap smear is used to detect cellular abnormalities.
This allows targeted surgical removal of condylomatous and/or potentially precancerous lesions prior to the development of invasive cervical cancer.
Although the widespread use of Pap testing has reduced the incidence and lethality of cervical cancer in developed countries, the disease still kills several hundred thousand women per year worldwide.
HPV vaccines Gardasil and Cervarix, which block initial infection with some of the most common sexually transmitted HPV types, may lead to further decreases in the incidence of HPV-induced cancer, however, they do not address the millions of people worldwide already infected with the virus.
It is estimated that nearly 10 million women are diagnosed with some form of cervical dysplasia each year in major global markets in the U.S., EU and Japan, many of whom could benefit from a non-surgical treatment.
As a result, HspE7 is first being developed for the treatment of CIN.