Acquired Immunodeficiency Syndrome (AIDS)

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Acquired Immunodeficiency Syndrome
Body Parts: Whole Body
Medical Subjects: Infectious Disease
Overview

What Is AIDS

AIDS virus, abbreviated HIV, is a virus that attacks the body's immune system. It takes the most important T4 lymphocytes in the human immune system as the target of attack, and devours and destroys a large number of T4 lymphocytes, thereby destroying the human immune system and finally collapsing the immune system, leading to the disease onset and death of the human body due to the loss of resistance to various diseases. Scientists call the virus the human immunodeficiency virus. The average incubation period of HIV in the human body is 12 to 13 years. People who look normal before they develop aids can live and work without any symptoms for many years.

Cause

What Is The Cause Of AIDS

AIDS is an infectious disease caused by human immunodeficiency virus (HIV), also known as HIV. It is worth mentioning that HIV itself does not cause any diseases, but when the immune system is destroyed by HIV, the human body loses its resistance and infects other diseases, resulting in death! Generally speaking, AIDS is a serious infectious disease in which the body's immune system is destroyed by HIV, which causes the body to lose the ability to resist life-threatening pathogens, causing multiple infections or tumors and finally leading to death. The virus is transmitted throughout life, destroying the human immune system and making the body lose the ability to resist various diseases. When the immune function of HIV-infected people is severely damaged by the virus and they are unable to maintain the minimum disease resistance, the infected people develop into AIDS patients. With the decline of human immunity, people will become infected with a variety of pathogenic microorganisms more and more frequently, and the degree of infection will become more and more serious, and eventually lead to death due to a variety of complex infections. AIDS is mainly transmitted through blood, improper sexual behavior, drug abuse and mother-to-child transmission.

Part 1. Effects of HIV Infection on CD4T lymphocytes

HIV viruses are retroviruses, so genetic information exists in two identical RNA single-stranded templates. The virus can bind to human cells with CD4+ receptors, especially can be combined with CD4T helper lymphocytes, can also bind to galactose ceramide on the surface of nerve cells. Reverse transcriptase can reverse transcription of viral RNA into DNA, which is then integrated with human genes. The viral DNA sequence is carry throughout life by infected cell and their offspring cells.

After entering the human body, HIV can selectively invade the lymphocytes with CD4 receptor, mainly CD4T lymphocytes. After HIV envelope protein gp120 binds to CD4 receptor on the surface of CD4T lymphocytes, with the help of gp41 transmembrane protein, the HIV membrane is fused with the cell membrane and the virus enters the cells. When the virus enters the cells, it quickly takes off its shell, in preparation for further replication. Recent studies have shown that in addition to the CD4 receptor, HIV entry into cells requires the interaction of cell surface proteases with the V3 ring of gp120.

The replication of HIV virus begins in the host cell. First, the two RNA strands are reversed into DNA by the virus reverse transcriptase, and then DNA is used as a template to replicate DNA under the action of DNA polymerase. These DNA parts remain in the cytoplasm. Low level replication is performed. Part of the DNA integrated with the chromatin of the host cell nucleus becomes proviral, and the infection enters the incubation period. After the latent infection stage of 2–10 years, when the infected cell is activated, the proviral DNA is transcribed into RNA under the action of transcriptase, which is then translated into protein. After assembly, a large number of new virus particles are formed, and these virus particles are released and continue to attack other CD4T lymphocytes. After a large number of CD4+T lymphocytes are attacked by HIV, the cell function is damaged and a large number of cells are destroyed, which is the cause of immune deficiency in AIDS patients.

HIV infection of CD4+T lymphocytes first causes cellular dysfunction. There were defects in recognition of and reaction to soluble antigens such as tetanus toxin, although reaction to mitogen phytohemagglutinin (PHA) remained normal. Decreased cytokine production, decreased IL-2R expression, and decreased ability to provide helper services for B lymphocytes. When HIV virus proliferates in host cells, it causes cell lysis and rupture. After intracellular replication of HIV, it can cause cell membrane damage when released by bud formation. HIV can inhibit the synthesis of cell membrane phospholipids and thus affect the function of cell membranes, leading to cytopathic effects. HIV can also infect bone marrow stem cells resulting in a decrease in CD4+T lymphocytes.

When the expression of gp120 present on the surface of HIV-infected CD4+T lymphocytes occurs, it can bind to the CD4 molecule of uninfected CD4+T lymphocytes to form fusion cells, thereby changing the permeability of cell membranes and causing cell lysis and destruction. The free gp120 can also bind to uninfected CD4+T lymphocytes and serve as an antigen for antibody-mediated dependent cytotoxicity, making CD4+T lymphocytes become target cells that are attacked and damaged by K cells. Gp41 transmembrane protein, which inhibits the proliferation of lymphocytes stimulated by mitogen and antigen, and thus causes the decrease of CD4+T lymphocytes. HIV infection generally begins with a mild to moderate decrease in CD4T lymphocytes, the total number of which can persist for years, and the reactive virus is suppressed by an immune response. Over time, CD4+T cells gradually declined in a progressive manner, indicating that the virus gradually escaped the control of the immune response. Opportunistic infections can occur once CD4+T lymphocytes have declined to 0.2×109/L or less.

Part 2. Effect of HIV Infection on Other Immune Cells

The impairment of immune function caused by HIV infection is not only the destruction of CD4+T lymphocytes, but also affects other immune cells to different degrees.

1. Mononuclear macrophages: Due to their surface CD4 receptors, they are also vulnerable to HIV invasion, but their infection rate is much lower than that of CD4+T lymphocytes. Studies have found that HIV-infected mononuclear macrophages have the effect of spreading HIV infection, which can carry HIV into the central nervous system. HIV infection in brain cells is primarily caused by mononuclear macrophages, such as microglia. The release of toxic factors by HIV-infected mononuclear macrophages can damage the nervous system. Impaired function of a certain number of mononuclear macrophages results in a decrease in the body's ability to fight HIV infection and other infections. Besides, the impaired CD4+T lymphocytes function is also related to the impairment of mononuclear macrophages function.

2. CD8+T-lymphocytes: CD8+T-lymphocytes have HIV-specific cytolysis. In the early stage of HIV infection, CD8+T lymphocytes have the effect of inhibiting virus replication and transmission. When the function of CD8+T lymphocytes is impaired, the condition of HIV infected people will develop. In the advanced stage of HIV infection, the number of HIV-1 specific cytotoxic T lymphocytes (CTL) gradually decreases, indicating that the loss of HIV-specific cytolytic activity of CD8+ T lymphocytes may be partly related to the reduction of CTL. The selective mutation of HIV and the destruction of CD4+ T lymphocytes are also the reasons for the loss of HIV-specific cytolytic activity.

3. B lymphocytes: after HIV infection, B lymphocytes can be activated by polyclonal antibodies, which increases the number of B lymphocytes in the peripheral blood and secretes immunoglobulins, thus increasing the levels of IgG and IgM. At the same time, the reactivity of B lymphocytes to new antigen stimulation is reduced. Therefore, as HIV infection progresses, purulent infection increases and antibody responses to the influenza A virus vaccine and hepatitis B vaccine decrease. For HIV infection, the mechanism of multiple activation of B lymphocytes is unknown, which may be due to the lack of regulation of normal T cells, the stage where B lymphocytes are activated by Epstein-Barr virus, or the direct activation of B lymphocytes by HIV.

Part 3. Factors Contributing to AIDS

After HIV infection, HIV replication at a very low level in the body is maintained for a considerable period of time, which is the long duration of the asymptomatic phase of AIDS. One of the reasons is that cellular immunity and humoral immunity can reduce the regulation of viral replication, and the other is that HIV enters CD4+T lymphocytes and becomes partially latent. Many studies have shown that some cytokines and other viral infections can activate HIV replication and expression, and there are reports that glucocorticoids and interleukins can synergistically enhance HIV replication. Tumor necrosis factors α, β, and IL-1 can also contribute to the expression of HIV, in particular TNF-α. Various genetic products of other viruses promote high-level HIV replication, and some viruses work with HIV-1 to destroy CD4+T lymphocytes. Therefore, in clinical practices, AIDS patients are often coinfected with cytomegalovirus, herpes virus, Epstein-Barr virus, human T-lymphocyte leukemia virus, etc., which in turn cause disease changes.

Part 4. Immune Response after HIV Infection

The immune system of the human body is the last line of defense against external infection. Many pathogens infect the human body and are finally eliminated through cellular immunity and humoral immunity of the human body. The immune system of the body plays a certain role in inhibiting the initial infection of HIV. However, with the damage of the immune system and the variation of HIV, the immune system of the body is finally helpless against HIV infection. HIV infection can stimulate the body to produce specific cellular immune response and the corresponding antibodies to various viral antigens. The body produces T-lymphocyte mediated cytotoxicity, and T-lymphocyte infiltration occurs in the brain of HIV infected individuals. Inhibition of HIV by CD8+T lymphocytes lyses HIV-infected target cells, suggesting that T cells play a role in inhibiting HIV replication in HIV infection. Antibodies produced by the body neutralize the free HIV virus and the HIV particles that bind to the cells but have not yet entered the cells. Natural killer cells and killer cells kill and lyse HIV-infected cells through antibody-dependent cytotoxicity. Cellular immunity and humoral immunity of the body can control the replication and spread of HIV for a period of time. However, due to the variation and recombination of the virus, it can escape from immune surveillance and cannot be completely cleared by the immune system of the body. When the immune system of the body is further damaged, under the action of certain triggering factors, HIV will be widely replicated and disseminated, eventually leading to the occurrence of AIDS.

Part 5. HIV Infection and Tumor

The increased incidence of Kaposi's sarcoma, B-cell lymphoma, Hodgkin's disease and certain tumors in HIV-infected individuals is directly related to the impaired immune function of HIV-infected individuals, but it may not be the only cause. The development of B-cell lymphoma in HIV-infected individuals is associated with EBV infection and HIV does not directly cause the tumor, as the presence of the viral sequence cannot be proven within the DNA of the tumor cell.

The pathogenesis of HIV infection can be summarized as follows:

1. After HIV invades the human body, it first binds to CD4+T lymphocytes that contain CD4 receptor on the cell surface, enters cells for replication, and partially integrates into cell chromosomal DNA to become latent.

2. The resistance of cellular immunity and humoral immunity to HIV in the body causes low-level replication of HIV at the early stage of infection.

3. Under the action of other factors, the latent HIV is activated and replicates in large numbers, widely invades CD4+T lymphocytes, and impairs the functions of CD4+T lymphocytes, mononuclear macrophages, B lymphocytes, CD8+T lymphocytes, NK cells, etc., finally leads to the whole immune function defect, and finally produces a series of refractory opportunistic infections and tumor.

Symptom

What Are The Symptoms Of AIDS

Clinical manifestations: The clinical manifestations of HIV infection include asymptomatic latent and severe opportunistic infections and clinical symptoms of tumor.

Part 1 Asymptomatic Incubation Period

After 2-12 weeks of HIV infection and 6-8 weeks of HIV infection, the anti-HIV antibody turned positive. At this time, a few people showed transient acute infection symptoms, including fever, rash, stiffness, enlarged lymph nodes, joint pain, myalgia, maculopapules, urticaria, abdominal pain, diarrhea and aseptic meningitis in some patients. White blood cells were normal, but monocytes increased, lymphocyte ratio decreased slightly, and platelets decreased slightly After that, it continued to be asymptomatic, which began to develop when the cellular immune function was low. The asymptomatic period lasted for 2-5 years and more than 15 years. Most adults and young people infected with HIV could be asymptomatic for a long time, but virus replication could be detected. With the damage of immune system and the increasing number of viruses, most people infected with HIV have related symptoms, such as burnout at the beginning, persistent fever, loss of appetite and unexplained weight loss, followed by diarrhea, night sweat, swelling of lymph nodes (first armpit, thigh, etc.). When HIV invades the central nervous system, dementia, forgetfulness and other symptoms often occur. AIDS-related complex (ARC) and persistent systemic lymphadenopathy (PGL) are called if there are only virus antibodies and no symptoms such as opportunistic infection peculiar to AIDS.

After 2-5 years after HIV infection, about 10% of the patients eventually developed into AIDS, and about 30% of them were ARC, while about 60% of them were asymptomatic HIV carriers, and about 15% of them developed into AIDS from ARC, so a large number of patients were asymptomatic carriers. This brings great difficulties to the prevention of AIDS.

Part 2 Classification of HIV Infection and Diagnostic Criteria of AIDS

According to the clinical manifestations of HIV-infected persons, they are divided into three types: A, B and C, and each clinical type is divided into three grades by CD4+T lymphocyte count. In the above three clinical classifications, except that all of them belong to AIDS, HIV-infected persons with CD4+T lymphocytes < 200/μl or CD4+T lymphocytes < 14% (i.e., A3 and B3) can also be classified as AIDS cases.

Note: The following classification has a premise and must be HIV-infected.

Classification A: Any one of the following three situations can be classified as Class A.

1. Asymptomatic HIV-infected persons

2. Persistent systemic lymphadenopathy

3. People with acute (initial) HIV infection diseases or medical history

Classification B: One of the following 11 cases is classified as Class B.

1. Hemangioma caused by Bacillus

2. Candidiasis of oropharynx (thrush)

3. Vulvovaginal candidiasis with persistent, frequent or poor treatment response

4. Cervical dysplasia (mild/severe)/cervical carcinoma in situ

5. Systemic symptoms lasting more than one month, such as fever (38.5℃) or diarrhea

6. There is hairy leukoplakia in the mouth

7. Including at least two obvious bursts or herpes zoster in the epithelial area

8. Idiopathic thrombocytopenic purpura

9. listeriosis

10. Symptomatic diseases of pelvic inflammatory disease, especially complicated with tubal and ovarian abscess

11. Peripheral neuropathy

Classification C: It includes 25 kinds of diseases with AIDS indications, and any one of them can be diagnosed as AIDS regardless of the number of CD+4T lymphocytes.

1. Candidiasis of bronchus, trachea or lung

2. Esophageal candidiasis

3. Invasive cervical cancer

4. Diffuse or extrapulmonary coccidiosis

5. Extrapulmonary cryptococcosis

6. Cryptosporidiosis causing chronic enteritis (course of disease > 1 month)

7. Cytomegalovirus diseases except liver, spleen and lymph nodes

8. Cytomegalovirus retinitis causing blindness

9. HIV related encephalopathy

10. Chronic ulcer caused by herpes simplex (course of disease > 1 month), or bronchi, pneumonia and esophagitis

11. Diffuse or extrapulmonary histoplasmosis

12. Chronic enteritis caused by isosporidiosis (course of disease > 1 month)

13. Kaposi's sarcoma

14. Burkitt lymphoma

15. Immune mother cell lymphoma

16. Primary lymphoma of brain

17. Diffuse or extrapulmonary Mycobacterium tuberculosis complex or Mycobacterium Kansas

18. Mycobacterium tuberculosis in any part (lung or extrapulmonary)

19. Diffuse or extrapulmonary mycobacteria of other species or unidentified species

20. Pneumocystis carinii pneumonia

21. Recurrent pneumonia

22. Progressive multifocal leukoencephalopathy

23. Recurrent Salmonella septicemia

24. Toxoplasma gondii

25. Wasting syndrome caused by HIV

Typical AIDS has three basic characteristics:

1. serious cellular immunodeficiency, especially CD4T lymphocyte deficiency.

2. There are various fatal opportunistic infection, especially Pneumocystis Carini pneumonia (PCP).

3. Various malignant tumors occurred, especially Kaposis sarcoma (KS).

PCP occurred in 64% of AIDS patients, and KS occurred in homosexuals and AIDS cases in Africa. The mortality rate of AIDS patients with PCP and KS is the highest.

Part 2 Common Opportunistic Infections Among AIDS Patients

Viral Infection

1. cytomegalovirus infection is a rare disease, but it accounts for about 90% of AIDS patients. It is a common complication of AIDS and an important complication of AIDS patients' death. Infection can affect the lung, digestive tract, liver, central nervous system and many organs. About one third of patients are complicated with omeningitis. The clinical symptoms are fever, shortness of breath, cyanosis, dyspnea, etc. The chest X-ray photos often show interstitial pneumonia changes, and diffuse frosted glass or reticular granular shadows can be seen in both lung fields. In the late stage, it develops into alveolar changes due to secretion storage in alveolar cavity. The antibody titer of AIDS patients to cytomegalovirus increases.

2. herpes simplex virus infection: the infection caused by herpes simplex virus (HSV) is related to the number of CD4T lymphocytes, and ulcer lesions, herpes carbuncle and other lesions are formed in the lips, pudenda and perianal regions, with obvious pain, and herpes pneumonia, digestive tract and herpes encephalitis can also be seen. Serological diagnosis is of little significance and can be confirmed by genetic diagnosis. Acyclic guanosine was used for treatment.

3. Herps zoster This disease is caused by Varicella-Zoster virus (VZV), and people under 50 years old with herpes zoster should suspect the possibility of HIV infection. Most patients in Africa present with facial herpes zoster and even develop omental necrosis. Treatment is the same as herpes simplex.

Bacterial Infection

1. Atypical acid-fast bacteria disease: AIDS patients complicated with bacterial infection, mostly systemic infection caused by mycobacteria. This disease has no conscious symptoms and no specific clinical manifestations. Some patients have digestive system symptoms such as night sweat, high fever, general weakness, diarrhea, abdominal pain and malabsorption. In addition, anemia and weight loss can also be seen. Diagnosis mainly depends on blood culture. Anti-tuberculosis drugs are often used for treatment, but they are often resistant to drugs. Because the infection is not life-threatening, symptomatic treatments such as anti-inflammatory, antipyretic and analgesic, and strengthening nutrition can be taken.

2. Tuberculosis: AIDS patients often have the recurrence of tuberculosis. Severe systemic infection outside the lung is common, and chest X-rays are normal. Because the immune system of AIDS patients is damaged, tuberculin reaction is mostly negative. Because most of them are systemic infections, tuberculous bacteria exist in feces, blood, urine, sputum and smears of biopsy specimens such as lymph nodes, lungs, liver, gastrointestinal mucosa and bone marrow, which is of great significance in diagnosis. Anti-tuberculosis drugs are available for treatment. Because tuberculosis can spread to healthy people through droplet infection. For suspected AIDS patients with tuberculosis, they should take Remifen for prevention.

Deep Fungal Infection

1. Candidiasis: Candidiasis is the most common opportunistic mycosis. It is outstanding in AIDS, which can cause esophageal candidiasis besides skin and superficial oral candidiasis. Weight loss and burnout may occur, and nonspecific digestive symptoms mainly include difficulty in swallowing and pain after sternum. Candida albicans can be isolated for diagnosis. In the basis of early diagnosis of AIDS, this disease occupies a very important position. Treatment, using antifungal agents, can improve symptoms, but easy to recur, showing refractory.

2. Cryptococcosis: The incidence rate of AIDS patients complicated with cryptococcosis is 6%, and cerebrospinal meningitis is the most common one, which can also be complicated with pulmonary cryptococcosis or cryptococcosis epicarditis. The main clinical manifestations are fever, headache, burnout, shame, mental state change, spasm and other symptoms. Cerebrospinal fluid examination is very important in diagnosis, such as increased protein and cell number, increased pulp pressure and decreased sugar.

Infection by Protozoa and Parasites

Pneumocystis carinii pneumonia: Pneumocystis carinii is one of the well-known typical opportunistic pathogens, which is usually parasitic in the alveoli of healthy people, but most of them are not dominant, and it is also a zoonotic disease. When its host immune function declines for some reason, it can reproduce and exert its pathogenicity. In AIDS, the immune system is damaged, which leads to Pneumocystis carinii pneumonia.

Pneumonia of Pneumocystis carinii is a very important opportunistic infection. 60% of AIDS patients are complicated with this disease, and 80%-85% will be complicated with this disease in the whole course. The initial symptoms are characterized by hypoxemia and progressive respiratory disturbance, especially asthma, dyspnea, dry cough, fever and other conscious symptoms during labor.

After relevant examinations, most of them were nonspecific infiltration shadows by chest X-ray, and 5% of them were normal. Pneumocystis carinii should be detected because of thick expectoration. When taking samples, the bronchoalveolar cells should be washed first, and lung tissue biopsy should be taken via bronchus or thoracotomy.

Treatment: Compound sulfamethoxazole tablet is the first choice, and its effective rate is almost the same as that of other immunodeficiency patients except AIDS, accounting for about 50% ~ 60%. However, the incidence of drug-induced fever, rash, leukocytes, thrombocytopenia, liver dysfunction and other side effects caused by this drug is relatively high, and almost 100% of patients die without treatment.

AIDS patients may also be complicated with sporidiosis. Such as amoebiasis, toxoplasmosis and recessive sporidiosis.

Part 4 AIDS Patients and Tumors

AIDS is one of the main causes of AIDS death due to immunodeficiency of immune function. It was confirmed in 1986 in the international research conference of Kaposis sarcoma (KS) and AIDS held in Nagataka, Japan that KS complicated with AIDS is different from the original KS, so the correlation between AIDS and tumor has attracted attention.

Kaposis Sarcoma (KS)

KS is the representative disease of AIDS malignant tumor. KS was first reported by Kaposis in 1872. According to the observation results of 3 patients, he described the clinical characteristics of KS, including idiopathic cutaneous sarcoma, multiple cutaneous sarcoma and pigmented sarcoma. It is considered to be a local frequently-occurring disease in the equatorial region of African continent. Under the local geographical conditions, it mainly affects middle-aged and old men, and most nodules of different sizes occur in limbs. Later, it is called Kaposis sarcoma.

KS invades a wide range of places, including limbs, face and trunk, skin, oral mucosa, eyelid and mucosa. In addition, lung, liver, spleen and other organs, especially digestive tract, are prone to massive bleeding. In a word, KS can occur all over the human body, and its clinical manifestations are as follows:

1. Nodular type: cherry red or purple, smooth surface, prominent skin surface, clear boundary and hard quality. Compression can reduce its volume and restore it to its original state within 10 seconds after relaxation. This sign is called Hayne's sign. Nodules can be distributed all over the body, but the most common ones are lower limbs, feet and forearms. Typical lesions are prone to bleeding, but there is no pain, and most patients are elderly. The survival period after illness is about 10 years.

2. Infiltration type, skin lesions fused with each other, ulcer or verrucous hyperplasia, often involving subcutaneous and bone tissues, this type mostly occurs in lower limbs and feet, and nodules exist in skin lesions. This type progresses rapidly, and the survival period is no more than 3 years.

3. Generalized type: It refers to the extensive invasion of internal organs and tissues except skin lesions, such as gastrointestinal tract, liver, spleen, respiratory tract and lymphoid tissues. When lymphoid tissue is invaded, it can be called lymphoid Kaposis sarcoma. Although generalized type accounts for only about 5% of all cases, it develops rapidly and has poor prognosis, which is often life-threatening due to massive bleeding.

Patients with KS sarcoma often suffer from malnutrition, and children may have rough skin, enterogenous acrodermatitis, scurvy-like skin lesions and severe aphtha. In addition, 50% of the patients were accompanied by thyrotoxicosis.

lymphoma

Non-Hodgkin's lymphoma in HIV infection is an index to diagnose AIDS. About 5%-10% of AIDS patients may develop non-Hodgkin's lymphoma, including primary cell lymphoma of brain. Most patients are poorly differentiated lymphomas, including small splinter cell type and large cell immune mother cell type. These patients often have extranodal lesions and often invade bone marrow, central nervous system, gastrointestinal tract, liver, skin and mucous membrane. Most patients show rapid lymph node enlargement, extranodal mass, or severe fever, night sweat and weight loss. Some patients often have primary lymphoma in central nervous system.

Diagnostic Basis

1. Epidemiology and clinical manifestations

2. Laboratory inspection

3. HIV antibody detection

4. Detection of HIV by PCR

Part 5 What Is The Earliest Identification Mark Of AIDS

HIV can suppress the immune system, resulting in skin diseases such as herpes, warts and mycotic infections. Skin symptoms may occur several months before the symptoms such as weight loss and fatigue appear.

Through further research and observation, the researchers found that a variety of serious and stubborn skin lesions can serve as early identification marks of AIDS infection. Contact with people infected with HIV, there will be related antibodies in the body. Studies have revealed that everyone with this antibody has one or several skin diseases as follows:

1. Herpes simplex blisters appeared around rectum and anus, and new warts were found in hands, feet and bearded parts.

2. Serious fungal infection in feet.

3. Skin inflammation, redness, blisters, accompanied by bacterial infections such as pustulosis, the typical performance is that a speckled blister appears around the mouth and nose.

4. Folliculitis appeared in the armpits and other areas.

5. Severe seborrheic dermatitis with severe oily scales on face, scalp and body skin.

6. Severe dry skin disease or young people suddenly have skin similar to that of old people.

Note: It must be pointed out in particular that although experts pointed out that the above skin diseases are early signs of AIDS infection, the condition is that patients should have the possibility of being exposed to the virus. These may include the recent import of suspicious blood, the use of biological products such as imported globulin of unknown origin, or the history of homosexuality and contact with AIDS patients. If these people suddenly have the above skin lesions, it is necessary to do further tests and make a definite diagnosis.

Part 6 Early Signs of AIDS (Oral Diseases)

According to international research and clinical experience, most AIDS patients will have oral symptoms alone within 1-4 years before the onset of AIDS. Oral diseases closely related to HIV infection are as follows:

Candida albicans: It occurs in the palate and back of tongue, and sometimes white spots or plaques can be seen in the red area. Or in any part of the mouth, showing white or yellow spots or plaques, which can be wiped away, leaving a red area with bleeding. Some people think that oral candidiasis and hairy leukoplakia can be used as predictors of AIDS.

Hairy leukoplakia: It is a white or gray lesion located on both sides of the tongue. The lesion can also extend to the abdomen and back of tongue, and the lesion cannot be removed. It is almost only found in HIV-infected persons and AIDS patients.

Periodontal disease: manifested as root inflammation, root ulcer, root necrosis, and loose teeth, and may have symptoms such as root bleeding, pain and stench. It is reported that 19%-29% of HIV infected or AIDS patients have periodontitis.

Kaposi's sarcoma: Single or multiple red, light blue or purple patches or masses with or without ulcer, which are found in the palate and root. Kaposi's sarcoma is very rare in normal people.

Detect

How To Check For AIDS

Ⅰ. The major cellular immunodeficiency above moderate level includes: CD4+T lymphocyte depletion: T lymphocyte function decreased, peripheral blood lymphocytes decreased significantly, CD4<200/μl, CD4/CD8<1.0 (1.25 ~ 2.1 for normal people), delayed allergic skin test was negative, mitogen stimulation response was low.

Ⅱ. B lymphocyte dysfunction: Polyclonal hyperglobulinemia, formation of circulating immune complex and formation of autoantibodies.

Ⅲ. NK cell activity decreased.

Ⅳ. Pathogen examination of various pathogenic infections, such as PCR. Histologically proven malignant tumors, such as KS.

Ⅴ. HIV antibody detection:

1. Enzyme-linked immunosorbent assay (ELISA)

2. Gelatin particle agglutination test (PA)

3. Immunofluorescence detection (IFA)

4. Western Blot (WB for short)

5. Radioimmunoassay (RIP)

Note: Among them, the first three items are often used in screening tests, while the latter two items are used in confirmatory tests.

Ⅵ. Detection of HIV by PCR.

Prevention

How To Prevent AIDS

Method 1 Specific Prevention

1. with the American CDC classification diagnostic standard in 1993, the diagnostic scope of AIDS has been expanded, which is beneficial to the prevention and treatment of AIDS. according to the decrease of CD4T lymphocytes, certain drugs should be given.

2. AIDS vaccines: Two AIDS vaccines containing gp120 were tested in the second phase in 296 people in the United States, and were temporarily stopped because 6 people had already been infected. UBI synthetic vaccine is being tested in Thailand.

3. Blocking mother-to-child transmission: AIDS pregnant women with CD4+T lymphocytes > 200/μl are treated with AIT before and during labor and infants, which has certain protective effect.

Method 2 Comprehensive Prevention

1. Popularize the knowledge of AIDS prevention, and understand the transmission route, clinical manifestations and prevention methods.

2. Strengthen moral education, prohibit promiscuity and unclean sex, and put an end to whoring.

3. Avoid sexual contact with HIV-infected persons, AIDS patients and high-risk groups.

4. It is forbidden to share syringes and needles with intravenous drug users.

5. When using imported blood, blood components and blood products, HIV testing must be carried out.

6. Domestic blood donors should be strictly selected, and they should be tested HIV-negative step by step to supply blood, so as to prevent HIV transmission.

7. Those who donate blood, organs, tissues and semen should be tested for HIV.

8. Establish an AIDS testing center.

9. Promote condom use and avoid anal sex.

10. people infected with AIDS or HIV should avoid pregnancy, and babies born should avoid breastfeeding.

The Main Route of AIDS Transmission

AIDS transmission is mainly through sexual behavior and the exchange of body fluids. Body fluids mainly include semen, blood, vaginal secretions, milk, cerebrospinal fluid and brain tissue of patients with neurological symptoms. Other body fluids, such as tears, saliva and sweat, exist in small quantities and generally do not cause the spread of AIDS.

Saliva is very unlikely to transmit HIV. Therefore, kissing generally does not spread. However, if a healthy person has a wound or a broken place in his mouth, and there is also a broken place in the mouth of an AIDS patient, if the two sides kiss, HIV may be transmitted through blood. Sweat will not spread HIV. Objects that AIDS patients have come into contact with cannot spread HIV. However, razors and toothbrushes used by AIDS patients may have a small amount of blood from AIDS patients; There may be semen on the towel. If you share personal hygiene products with patients, you may be infected. Patients who get AIDS because of promiscuity often have other sexually transmitted diseases. If they share personal hygiene products with them, they may be infected with other diseases even if they are not infected with AIDS. Therefore, personal hygiene products should not be shared with others.

General contact can not infect AIDS, so AIDS patients should not be discriminated against in their lives, such as eating together and shaking hands will not infect AIDS. The food and soup that AIDS patients have eaten will not infect HIV. HIV is very fragile. If it leaves the human body and is exposed to the air, it will die within a few minutes.

1. Sexual intercourse transmission

2. Blood transmission

3. Spread of shared needles

4. Mother-to-child transmission

Although AIDS is terrible, its transmission power is not very strong, and it will not spread through our daily activities. In other words, we won't be infected with AIDS because of kissing, shaking hands, hugging, sharing meals, office supplies, sharing toilets, sharing swimming pools, sharing telephones, sneezing, etc. It doesn't even matter if we take care of people infected with HIV or AIDS.

Extension: Why Don't Mosquitoes Infect HIV

Mosquito bites may spread other diseases (such as yellow fever, malaria, etc.), but they will not spread HIV. Because, when they bite a person, they don't inject blood into themselves or the person who has been sucked in front of them. Instead, they inject their own saliva, which can prevent this person's blood from naturally coagulating. Moreover, HIV will only survive for a short time in insects, and will not multiply continuously in insects. Insects themselves don't get AIDS.

Susceptible Population

1. Gay men

2. Intravenous drug addicts

3. Hemophilia patients

4. Recipients of blood transfusion or blood products

5. People who have sexual relations with high-risk groups

6. Other high-risk groups of AIDS

Treatment

How To Treat AIDS

At present, there is no specific treatment for viral infectious diseases, so there is no effective treatment for AIDS. In addition, the integration of HIV virus nucleic acid with host chromosomal DNA and replication by host cells bring difficulties to drug treatment. Early treatment of HIV infection is very important. Treatment can slow down the decline of immune function. The risk of tuberculosis, bacterial pneumonia and pneumocystis carinii pneumonia among HIV-infected people is increasing, so early prevention is very important.

Method 1: Support Therapy: improve the progressive consumption of AIDS patients as much as possible.

Method 2: Immunomodulatory Therapy.

1. Interleukin-2(IL-2): It can enhance the cytotoxicity of MHC-restricted cells infected by HIV, and also enhance the activities of natural killer cells (NK) and lymphokine-activated killer cells (LAK) which are not restricted by MHC.

2. Granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF): increase circulating neutrophils and improve the anti-infection ability of the body.

3. Lingberin: It activates the pituitary gland, that is, adrenal cortex system, adjusts the internal environment and functions of the body, enhances the body's adaptability to changes in the external environment, stimulates the body to produce humoral antibodies, increases the total number of white blood cells, strengthens phagocytosis, and activates the body's defense system to resist the invasion of pathogenic microorganisms and viruses.

4. Interferon (IFN): IFN):α- α can slightly increase CD4+T cells in some patients, and 40% of Kaposis sarcoma patients have tumor regression. Interferon-β (IFN-β), given intravenously, has a similar effect to IFN-α, but its anti-Kaposis sarcoma effect is weak when injected subcutaneously. Interferon-γ (IFN-γ) can improve the activity of monocytes and resist Toxoplasma gondii and other conditional infections.

Method 3: Antiviral Preparation.

1. drugs for inhibiting HIV binding to host cells and penetration: soluble rsCD4 can bind to HIV and occupy CD4 binding site, so that HIVgp120 cannot bind to CD4 on CD4T lymphocytes and penetrate into infected CD4T lymphocytes.

Dose: rsCD4 clinical trial 30mg/ day, intramuscular injection or intravenous injection, continuous 28 days.

2. Drugs for inhibiting HIV reverse transcriptase (RT): By inhibiting reverse transcriptase, HIV replication is blocked. The effective drugs are azidothymidine and dideoxycytidine.

Identify

How To Identify AIDS

AIDS patients often have obvious weight loss, severe malnutrition, anemia, leukopenia, platelets or whole blood cells.

Long-term diarrhea causes water and electrolyte disturbance, and nervous system damage causes mental decline, unresponsiveness, depression, anxiety, paranoid psychosis or dementia.

The damage of cardiovascular system causes tachycardia, cardiac enlargement and congestive heart failure.

Renal damage can cause interstitial nephritis and tubular necrosis, and lead to proteinuria, oliguria, high edema, azotemia and renal failure.

The damage of musculoskeletal system can cause wandering arthritis, joint pain and joint cavity effusion, which is similar to rheumatoid arthritis, and has poor anti-rheumatic treatment effect. It can also show polymyositis, obvious tenderness and dyskinesia of muscles, and necrotizing myositis in muscle biopsy.

The damage of endocrine system can cause adrenal insufficiency and hyporenia, hypotension, persistent hyponatremia and hyperkalemia, hypothyroidism, diabetes and adrenal crisis.

Complication

What Are The Complications Of AIDS

AIDS patients often have obvious weight loss, severe malnutrition, anemia, leukopenia, platelets or whole blood cells.

Long-term diarrhea causes water and electrolyte disturbance, and nervous system damage causes mental decline, unresponsiveness, depression, anxiety, paranoid psychosis or dementia.

The damage of cardiovascular system causes tachycardia, cardiac enlargement and congestive heart failure.

Renal damage can cause interstitial nephritis and tubular necrosis, and lead to proteinuria, oliguria, high edema, azotemia and renal failure.

The damage of musculoskeletal system can cause wandering arthritis, joint pain and joint cavity effusion, which is similar to rheumatoid arthritis, and has poor anti-rheumatic treatment effect. It can also show polymyositis, obvious tenderness and dyskinesia of muscles, and necrotizing myositis in muscle biopsy.

The damage of endocrine system can cause adrenal insufficiency and hyporenia, hypotension, persistent hyponatremia and hyperkalemia, hypothyroidism, diabetes and adrenal crisis.

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