During the first 2 to 4 weeks of infection, high titers of free virus are present in the circulation, and high titers of viremia are often accompanied by highly potent p24 antigen and blood viral loads of up to 1,000,000 copies/mL. The peak of viremia is also often accompanied by the onset of clinical symptoms. Antigen-antibody responses can be monitored 6 weeks after infection with the virus. Anti-gp160 and anti-p24 are detected first, followed by anti-gp120 and anti-gp41. antibodies to the viral envelope (e.g., gp120 and gp41) can be carried throughout life, but the anti-p24 antibody response may be converted to P24 antigenemia later in the course of the disease, or both may be negative. The quality and quantity of specific HIV cellular immune responses during acute infection, especially cytotoxic CD8+ T lymphocytes, are also host factors that influence the natural history of HIV infection. It takes about 6 weeks or more for the body to produce detectable antibodies, a period known as the “window period”. This transition period is also known as the seroconversion period, during which p24 antigen testing and HIV RNA testing are important. Current research is uncertain whether therapeutic interventions during acute infection are beneficial to patients, and the amount of plasma HIV RNA in the early post-infection period is the best predictor of disease course. The following two studies are supportive of early antiretroviral therapy. One study showed that zidovudine (AZT) alone in patients in the acute phase altered the clinical course of HIV infection and helped protect patients’ immune function compared with placebo. In addition, acute-phase patients given HARRT had more dramatic results, with viral loads in their blood and tissues reaching undetectable levels and lasting for more than 1 year. Although prolonged viral suppression does not mean that the virus is eradicated, for this subset of cases, sustained suppression of viral replication may significantly alter the course of the natural history of HIV infection. Early therapeutic intervention when the virus has not yet mutated and immune function is still intact is theoretically beneficial, and ultra-early (pre-seroconversion) potent antiretroviral therapy can maintain HIV-specific CD4+ T lymphocytes in a proliferative state, a response similar to that of long-term nonprogressors. Laboratory diagnosis in the acute infection phase: a. Negative to positive p24 antigen and anti-HIV antibodies within six months based on history; b. 4-fold increase in antibody titer; c. Negative antibodies and positive p24 antigen and nucleic acid tests. Although the diagnosis can be made directly at this stage, it is still very difficult to detect this group of cases as quickly and efficiently as possible. Primary HIV infection with first onset is often overlooked clinically, and patients in the acute phase often present with a syndrome of “viral illness”. Most of these symptoms are transient and non-specific. It is estimated that only 20-30% of these patients actually seek medical help, and even specialists may often miss these cases. After the initial infection, more than 40-70% of patients in the acute phase have influenza or mononucleosis-like symptoms, which may include fever, headache, sore throat, erythematous rash, diarrhea, and enlarged lymph nodes. Fever is most common, followed by lymph node enlargement, pharyngitis, or transient measles-like rash. The types of these symptoms and their relative incidence are shown in Table 2. Manifestations of immunodeficiency are even observed in this period: oral candidiasis albicans, esophageal candidiasis, etc., and even Pneumocystis carinii pneumonia has been reported in the acute infection period. The reason for this is the very low absolute CD4+ T-lymphocyte counts in these acutely infected patients (15% below 399, 7% below 300 cells/mm3 ). Certain oropharyngeal signs or symptoms including pharyngitis, painful swallowing, oral or tonsillar ulcers, and idiopathic esophageal ulcers can occur during this phase. Neurologic manifestations, although uncommon, have been reported, such as virtual meningitis (with or without increased cerebrospinal fluid cell counts and positive cerebrospinal fluid cultures), peripheral neuropathy, myelopathy, brachial plexus neuritis, facial nerve paralysis (Bell’s palsy), and, less commonly, self-limiting encephalitis and Guillain-Barre syndrome. The first symptoms tend to occur 2 to 6 weeks after being infected, with symptoms lasting 2-3 weeks before resolving on their own in the acute phase, which is the most contagious. Often the duration of these symptoms varies widely. One study has suggested that fever and headache last an average of 16.9 and 25.8 days, respectively, in patients in this phase. Acute seroconversion symptoms that last too long have been associated with rapid progression to AIDS. Integrating these symptoms into a fully defined syndrome (e.g., attributing fever, sore throat, and cervical lymph node enlargement to “mononucleosis-like”) is of little help in screening cases. Repeated prolongation of nonspecific symptoms can be used to rule out HIV infection. Laboratory manifestations of acute seroconversion are characterized by lymphopenia and depletion of CD4 and CD8 cells, with a rise in CD4+ T-lymphocyte counts, followed by a rapid, transient decline, and a drop in the CD4/CD8 ratio to 0.5 or less (normal is about 2:1). Abnormal lymphocytes are often seen in 20% to 30% of the peripheral blood, and anemia and thrombocytopenia may also be seen. The initial lymphopenia is followed by a predominantly CD8-cell lymphocytosis, and when the acute seroconversion syndrome resolves, the CD8 lymphocytosis returns to normal; although CD4+ T lymphocytes are also rising at this time, they are not able to return to their initial levels. In some cases, CD4+ T lymphocytes remain suppressed and do not show a rebound effect. If a patient shows a dramatic decrease in lymphocytes, this usually indicates an accelerated progression of HIV disease.